Insect Ecology
ENT54306, Wageningen University and Research, February/March 2022
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A lot of the insects have an association with plant species  co-evolution with plants  these two groups of
organisms influence each other’s evolution
o Insects attack plants  plants evolve to protect itself  some insects evolve to become resistant to
protection of plants  a lot of diversity between plants and insects
By looking at the damage on fossilized leaves  evidence of insect activity  compare damage to the damage
on today’s leaves  what species were there
Ca 1 million known species, 6 mil estimated
Insect body plan: gives an indication on how the
insect plays a role in ecosystem, what/how it eats,
how does it lay its eggs, etc...
Surface-volume ratio: surface 2D, volume 3D, with
increasing size  the volume increases faster than
surface,  increasing problems with diffusion of
oxygen,  increasing problems with exoskeleton
o Small size: how to cope with reduction
in organs, especially brain size  do
small wasps have relatively much
larger brains than large wasps?
 Trichogramma evanescens has
body size variation: when
parasiting a small egg the wasp
will become very small, three
iso-female strains
o Microscopy: measure the head and brain with scanning the insect head (brain in relation to body size) 
expectation: relative size would be bigger for smaller wasps  actual: linear regression, when the body
becomes smaller the brain becomes smaller too  are the tiny vs big wasps equally able to memorize
where an egg is?  no difference  dramatically different brain sizes but has the same functions and
number of cells
Exoskeleton and insect size: molting (vulnerable stage) to
become larger (constraint of collapse under body weight when
shedding skin)
Gas exchange and insect size: trachea system (small holes on the
outside (spiracle) of the skin), diffusion is quite cost heavy  harder to
bring oxygen to the right part of your body when you become larger
Different flight mechanisms in different insects ------------------>
!Exam: what is the constraint in insects in becoming so large
(exoskeleton, oxygen) try to link it to the body plan of the insects (why they become smaller)
Larval stages with the different size have different places in the food chain and in ecology
o Holometabolous: species that have very similar larval stages, might molt into different stages, have a true
pupil stage with a large metamorphosis to become the true adult
o Hemimetabolous: species that look more and more like the adult version with each stage
o Four major categories of insect feeding specialization (animal – plant – solid – liquid)
Food web structure with trophic levels and interactions, community complexion
o Hyperparasitoids: not much energy is lost when going a trophic level up  can result in very high trophic
levels (however, timing must be very right)
o What makes the interactions in the food web? Indirect interactions?  herbivore species can have
specialized parasitoids, going up the trophic levels the amount of parasitoids go up as well
o Plant quality: might result in different food webs, e.g. aphids become larger  attract different parasitoids
Ecological services of insects: removing dung, pollination, controlling pests, food  no life without insects
Mutualism and Symbiosis
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Major transitions in evolution: cooperation between lower-level units to form new higher-level units  e.g.
o Independent DNA molecules  longer molecules
o Prokaryotic cell  eukaryotic cell (endosymbiosis)
o Single cell  multicellularity
o Single individuals  social groups
o Single species  mutualism
Endosymbiosis: Mitochondria and chloroplasts descend from free-living bacteria: own DNA, independent
protein-synthesising machinery, ribosomes resemble bacterial ones
o Chloroplasts have been acquired via a series of endosymbiotic events  a couple times have cells
engulfed other cells, happened multiple times, can see because of the amount of membranes around it
Mutualism: an association between two species, beneficial for both (++)
Symbiosis: intimate interaction between different species (parasitic, neutral, mutualistic)
There’s usually a division of labour, sometimes both partners doing the same, but together more efficiently than
alone  predator satiation (gregarious reproduction to satiate predators of offspring), mixed-species bird flocks
Mullerian mimicry: a different species evolves to have the same colouration and toxins (or without toxins  one
benefits and cheats the system)
Trade: two partners both need a product, one is better or cheaper at producing one and the other at producing
another  if both partners can buy each other’s product both benefit  mutualism more likely to evolve
between members of different kingdoms
Symbiosis versus brief exchange:
o Symbiosis: long-term close relationship (‘long-term business contract’)
examples: fungus-growing insects, mitochondria/chloroplasts, Buchmera
and aphids
o Brief exchange: constantly changing interactions (‘buyer and shop’),
examples: seed dispersal, pollination
The outcome of interactions is not black and white and can vary with circumstances
o Social aspect of symbiosis: group of symbionts ------------------------------------->
Tragedy of the commons problem: group of symbionts share a resource, individual
success at the cost of the group is possible  prisoner’s dilemma
Two lower levels of selection: between species within the mutualism, between
individuals within a group of symbionts, levels are interrelated because the host is
interested in group success of its symbionts  host should maximise the group
component of symbiont fitness
Optimal sex ratio varies with number of foundresses
o Fig wasps: mating occurs locally within the fig, males die upon mating, only daughters disperse, single
foundress  son competes with brothers for access to mates (local mate competition), additional sons
are reproductively redundant, single foundress maximizes her number of grandchildren by producing
mostly daughters and only enough sons to ensure fertilization
 Yet if >1 foundress: competition between sons and other sons  mother has an interest in
producing extra sons  sons are not in the interest of the fig  more sons, less daughters 
reduced group productivity of the wasps  sons do not disperse pollen but do consume seeds 
therefore causes a decreased fig (host) fitness  male wasps are competitive ‘virulent’ trait
favoured to increase in response to declining relatedness
o Host-symbiont conflict  host tree: few foundresses per fig (increases relatedness and favours a rise in
allocation to females)  wasps compete for colonization of figs  increase number of foundresses per
fig unless controlled by trees  experiments have shown that trees seal off a fig soon after the first
foundress wasp has entered
 Maximise group success of symbionts: Increase symbiont relatedness via ‘weeding’ of genetic
diversity, increase symbiont relatedness (kin selection)  via vertical transmission (bottleneck)
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Vertical uniparental transmission: increases within-host relatedness between symbionts and thereby increases
importance of kin selection (number of symbionts transmitted important), symbiont fitness aligned with host
fitness  No guarantee for mutualism and horizontal transmission can also lead to mutualism
Reduce correlation between symbiont competitive abilities and reproductive success
o Sanctioning: nitrogen fixing bacteria  tragedy of the common, some nodules don’t produce N but take
nutrients  plant can ‘punish’ these by not giving them nutrients
o Early germ-soma split
Summary
o Distinction mutualism-parasitism gradual
o ’Division of labour’ versus ’doing the same’
o Symbiosis versus brief exchange
o Often, a symbiotic entity consists of a single host and multiple symbionts
o Here, two lower levels of selection than the mutualistic unit exist:
 Between species vs. Between symbionts within the host
o An important question for those symbioses is how the host can maximise the group success of symbionts
o Co-speciation and transmission patterns
Darwinian Agriculture
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Too-much-talent effect: there is an optimum of the percentage of top talent  Darwinian agriculture seeks to
avoid this  competitive characteristics can decrease yield
o Trade-offs between individual competitive traits and collective performance affecting yield not always
bad  other forms of agricultural symbiosis may have undiscovered principles of sustainable agriculture
How do termite farmers select crops? Maximize yield? And maintain high yield?
o Transmission mode: where do the new colonies get their fungus?  colony did not grow fungus and had
to get it from an external input  where do they get them from? Mushrooms (usually spawn a bit later
than the flying of termites, once a year)
Fungus-growing termites are ruminants  complementary symbiont contributions to plant decomposition in a
fungus-farming termite  gut passage may prepare substrate for specific fungi  gut bacteria?
Maximizing yield
o Fungus-growing termites grow their fungi in monoculture, despite horizontal acquisition via sexual spores
 termites prevent competitive interactions between different strains
 Varying outcomes of interactions between fungi
 Yield is positively correlated with relatedness of the fungi
o Monoculture: maximizes productivity, is stable (ecologically), and will favour mutualism with termites
How to maintain yield and avoid too-much-talent-effect of their nuclei?
o ‘Too-much-talent’ is cheating  a fungal mycelium is a colony of nuclei: some altruistically give up
reproduction in favour of other nuclei that end in spores, all nuclei are hopeful reproductive, mycelia can
fuse  share a common cytoplasm  becomes a public good  prone to tragedy of the commons 
everybody suffers  what do termites know that we don’t?  cultivated fungi for 35 mil years
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Less ‘anarchy’ in mycelium than in Neurospora. Termitomyces has cell compartments, consisting
of two nuclear types (Nobre et al., BMC Evol. Biol. 2014)
 Sufficient testing at mycelial level (depends on density of inoculation)
 Compartmentalisation of fungus garden, so that local decrease in productivity is not ‘infecting’
whole fungus garden (most species have multiple separate fungus gardens)
 ‘Serial monogamy’: take-over by more productive ‘foreign’ fungus, once productivity drops
Ancestral predisposition (ancestor had similar growth cycle of underground asexual cycle on insect faeces)
towards a domesticated lifestyle in termite cultivated fungus Termitomyces
Competition
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Evolution through natural selection: 1. Variation among individuals, 2. Competition, 3. Natural selection 4.
Currency = fitness or body building
2 mechanisms of competition:
o Exploitative competition: by using resources, some individuals deprive others of benefits to be gained
from resources  compete for same resource without physically interfering
o Interference competition: individuals harm each other directly through fighting, killing or indirectly by
aggressively maintaining a territory or producing chemicals that deter other individuals
Interspecific competition: between individuals of different species, intraspecific = same
Competition:
o Weak effects on insect body size and plant damage
o Moderate effects on abundance, survival, development time and
relative growth rate
o Large effects on fecundity and oviposition preference
Herbivores: phylogenetic similarity between competing species = poor
predictor of strength of interactions among chewing insects, competition
weaker between congeners (organisms within same genus) than between
more distantly related chewers  contrary to expectation of traditional
competition theory, competition often asymmetrical
Induced resistance as a factor in plant-mediated competition between insect herbivores
o Induced resistance: plants change according to damage done  results in plant mediated competition
Spatially heterogeneous effects: plant-mediated
competition is not homogeneous
o When changes occur in leaf number 5 you also
see an effect on leaf number 10 ------------------->
Effects of damage can be long-lasting
Induction effects create variation in the environment:
spatial variation, density variation (neither linear), time
needed for induction and for extinction – time can be
long, plant-mediated competition between herbivores
is spatially and temporally variable
Apparent competition: density of one resource species affects density of
consumer that subsequently affects density of a second resource species
 interactions through natural enemies ---------------------------------------->
o Trophic cascades: carnivore abundance, affects plant abundance,
stronger in ‘linear’ food webs (e.g. parasitoid  host  plant), reticulate
food webs dampen effects
o Carnivore removal in food web: direct positive effect on
herbivores  indirect negative effect on plants (biomass,
damage, reproductive output)
o Non-trophic interactions are very important for avoidance of cascading extinctions  complex systems
are more stable than simple systems
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Competition among parasitoids
o Strong mandibles in larvae of solitary parasitoids (one egg is lain in a host)  outcome of competition is
size-dependent
o Some hosts not completely defenceless: by encapsulating the larvae of the parasitoids in aggregated
haemocytes the larvae suffocates  Some parasitoids inject a virus when laying an egg in a host (virus –
parasitoids symbionts)  virus eliminates the encapsulation response of the host  virus blocks
everything so cross protection to other parasitoids  facilitation and competition of virus larvae
Competition even between parasitoids when they each inhabit a different host on a different leaf on the same
plant  plant-mediated competition (plant changes as a response to the caterpillar hosting a certain parasitoids
and this effects the mortality of other caterpillars with certain parasitoids)
o Plant-mediated competition: not restricted to herbivores but also between parasitoids that live in
herbivores, not restricted to same location or same time of feeding, also examples of aboveground vs
belowground competition
Sometimes species help each other even though they compete (e.g. caterpillars and aphids)  induced
facilitation (has effects on their respective parasitoids)  need knowledge of mechanisms underneath
Degree of variation as indicator of severity of competition  e.g. species diversity of ants increase (more
competition)  variability in mandible length decreases (everybody grows bigger mandibles)  strong selection
due to competition OR mandible sizes of other species of ants vary from site to site such that they always differ
from those of local competitors  it pays to specialize
o Competitive displacement in Aphytis parasitoids: minimum host size for production of female offspring
larger for inferior competitor (host needs to be a bigger size to grow female reproductive organs) 
displacement of this species (dependent on availability of host) to different Aphytis species because it
needs less host size  inferior competitor parasitises smaller hosts
Summary
o Exploitative vs interference
o Modifies interactions in food webs and enables coexistence
o Modifies community dynamics
o Short term as well as long term consequences for population dynamics, community dynamics
Parasitoids
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Parasite vs parasitoid
o Parasite: lives in symbiosis with a phylogenetically unrelated organism over a prolonged period of time,
lives in or on host, obtains nourishment from host without preventing host form reproducing, cannot live
independently, relationship lasts the lifetime of host, usually more than one generation
o Parasitoid: spends a significant portion of its life history attached to or within a single host, lives in or on
host, ultimately kills and often consumes host, obtain nourishment from host but is not needed to survive,
can live independently, relationship lasts the lifetime of host, host usually dies before it can reproduce
Characteristics parasitoid: specialized in choice of host (and host life stage), smaller than host, only female
searches for host, different parasitoid species can attack different life stages of host, adults are free-living,
mobile, may be predaceous, eggs or larvae usually laid in, on or near host, immatures remain in or on host and
almost always kill host  parasitoids attack host eggs, larvae, pupae and adults  yet specific to one host stage
o Specialized lifestyle because parasitoid adapts to host and immune system of host
Different lifestyles parasitoids
o Ectoparasitoid (living outside host, no immune system to adapt to, but if host molts you need to reattach
or you lost the host) vs endoparasitoids (living inside host)
o Idiobionts (living their own life – parasitoid kills or paralyzes host, prevent any further development, host
life stage is made immobile  egg, pupa, paralyzed larva) vs koinobionts (sharing life with host – host
continues to feed and grow until completion of parasitoid development, feeds on non-crucial tissues)
o Solitary (only one egg can successfully develop in host vs gregarious (more eggs deposited and
successfully developing in host)
o Pro-ovigenic: all eggs are ready upon emergence of parasitoid from pupa vs syn-ovigenic: parasitoid
emerges with limited number of eggs developed and needs protein food source to develop further eggs
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Different forms of parasitism
o Superparasitism: two parasitoid individuals of the same species attack the same
host individual
o Multiparasitism: two parasitoid individuals of different species attack the same
host individual
o Hyperparasitism: parasitoid parasitizes (can be in or on) another parasitoid species
within the host
o Heteronomy: parasitoid that parasitises its own species to make a male  male
parasitoid develops within a female conspecific individual within host
Cotesia glomerata parasitizes early instar Pieris brassicae larvae then continue to develop  4th of 5th larval
instar the parasitoids egress to pupate outside the caterpillar  after larvae get out of caterpillar, they make a
cocoon  caterpillar is still alive and will defend this cocoon, it dies after wasps fly out
Host size for solitary parasitoid wasps
o Host size variation  offspring fitness variation, increase in body size  more benefit to females, females
should produce sons in relatively small hosts, daughters in larger
o Host discrimination: rejecting parasitized hosts
o When competitors are present the wasps stayed longer and they superparisitized more  self
superparisitization: laying two eggs of yourself in one host  beneficial because: overcoming
encapsulation response, enhancing competitive power with other parasitoid individuals
Three phases in host searching
1. Host-habitat searching: reliability-detectability problem for parasitoid  tiny host: high reliability but low
detectability, effects on environment: low reliability but high detectability  solution through
association: herbivore-induced synomone (plant volatiles), (high reliability, high detectability)
 Chemicals in spit of caterpillar is perceived by plant  plant produces volatiles  volatiles attract
the parasitoid  can even perceive which hosts are on the plant  wasps learn (associative
learning)  Learning: effect of previous experience on behaviour, fast and slow learners
2. Host searching
3. Host acceptance: right species, parasitized or not, etc.
Parasitoids exposed to what their hosts feed on: glucosinolate content in cultivated and wild cabbage (Brassica
oleracea)  glucosinolate amount increases in wild variant when eaten by caterpillars  generalist caterpillars
are killed by this increase and in specialists development is slowed
o Previous infestation increases defence in plant  specialist herbivore is affected in another way too: less
energy available for encapsulation
Summary
o One host and that is it  careful host selection
o Use of herbivore-induced plant volatiles to locate hosts
o Host selection in host patch
o Host discrimination: parasitized from unparasitized hosts
o Competition within host
o Host quality dependent on food of the host
o Host quality dependent on other parasitoids, now and later
Predators
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Predators: Consume more than one prey per predator, usually larger than prey (not always, if smaller usually
take down prey in groups/larger numbers), usually more generalistic than parasitoids, may be omnivorous
o Polyphagous (generalist, omnivore) vs monophagous (specialist, carnivore)
Prey quality in terms of development time, mortality, reproductive quality offspring, sometimes nutritional
advantages (e.g. beta-carotene)
Diapause: state of physiological inactivity, induction by shortened days, termination of diapause cannot be done
unless state of diapause has lasted for several months, termination usually induced by higher temperature plus
long days (longer light)
o Predatory mites: induced by several short days in a row, beta-carotene required for short day perception
Odour preference: herbivore-induced plant volatiles  the more the plant is harmed by the herbivore  the
more plant volatiles plant produces  the more predators will be able to detect this
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You can find out what a predator has been feeding on by looking at what is in its gut
Bigger prey are often preferred by predatory mites (Typhlodromus piri, Amblyseius andersoni)  they
make decisions about who they want to feed on
 Amblyseius andersoni: when in need of carotenoids they were attracted to a much larger group of
prey than when not in need of carotenoids  responses and decisions that predators make is
dependent on the need for certain nutrients (and more factors)
Predators can solve their reliability-detectability problem by making use of herbivore-induced plant volatiles
o They exploit the chemicals in finding prey, can perceive prey presence, identity and quality, respond
according to their needs
Sitting and waiting: ant lion, praying mantis
Use of cues in active foraging (e.g. herbivoreinduced plant volatiles)
o Different walking patterns of active
foraging -->
Insect predators don’t always prey on other
insects
Prey defence against predators
o Chemical defence: e.g. bombardeerbeatle,
mixing hydroquinones plus hydrogen peroxide
with oxidative enzymes, leading to pbenzoquinone at a temp of 100°C
o Group defence: advantage: some prey survive/predator can’t eat
everyone, disadvantage: easier to find, more exploitative competition
o Sequestration of plant toxins: e.g. cardenolides by monarch butterfly,
mimicry of other butterflies to take advantage of the fact that the
monarch is toxic, mimics that are toxic support the system
o Mimicry to disguise: mimic to look like a predator
Predators reduce numbers of prey a lot more than
parasitoids, numbers never constant
o Effects on prey population: Huffaker’s population
dynamics experiment: spatial heterogeneity is
crucial: hiding places and such  otherwise
predator (nearly) exterminates prey
Interguild predation: predators eating predators
o Predatory mites feed on gall midge larvae 
reduce predation on aphids by gall midge larvae  gall midge adults lay
more eggs (on plants with higher aphid densities)
Predator avoidance by prey: avoiding places predators have been
o Usage of direct cues: smell of predator present
o Usage of indirect cues: dead adults and/or eggs present (mites given a
choice between pierced adults or frozen (intact) adults  they would choose to go to the intact adults)
o Spider mites avoided omnivorous predators that were feeding on mites more than same omnivorous
predators that were feeding on pollen  mites can differentiate between what a predator has eaten 
has maybe something to do with animal protein being present in/on predator but is not known
Foraging behaviour and conflicts: good food source with predators or bad food source without predators 
bean = good, tomato = suboptimal  will go about 50-50
o Reared on bean or tomato (over generations): reared on tomato will go more towards the tomato, reared
on bean will go more towards bean with spider mite extract (cue for predation)  conditions when
growing up influence what the mites do
Non-consumptive effects of predators: more mortality of caterpillars when predator with non-functional
mandibles  because of less feeding in presence of predator/stress?
Kleptoparasites: steal the prey of someone else
o Spider kills honey bee  flies feed on honey bee  flies are major pollinators of pitfall flower  flower
mimics the bee volatiles (odour of dead bee) to attract flies  flower exploits kleptoparasitic behaviour
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Summary
o Usually larger than their prey
o Polyphagous but prey preference
o Prey quality in relation to fitness
o Intraguild predation
o Prey defences
o Prey avoidance of predators
o Non-consumptive effects
Reproduction
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Bringing together the sexes
o Swarming: in the air – usually above a landmark, competition and selection going on in the air
o Leks: substrate based, individuals of one sex (usually males) aggregate and incoming female selects
o Pheromones: sometimes parasitoid/predator can also pick up on/create these pheromones
o Sexual selection: sometimes male put to test before mating (male moth feeds on plant with toxins,
creates pheromone with this, female selects these males  male gives female this toxin, female uses it
to put it on the eggs so they are protected)
o Courting process: female can still reject the male  male put to test (e.g. resistant vs non-resistant male
to toxins (cantharidin) in meloid beetles (Spanish fly)  male sequesters cantharidin from food and
protects the eggs with it so they’re chemically protected  advantage for female
 Nuptial gift: male gives gift, female eats gift, male fertilizes female
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Making sure no other male mates with her ↑
o Male plugs female tract on which female can feed, no other males can fertilize her
o Sometimes male transfers substance form male accessory gland that makes female unreceptive
o Mate guarding: investment of time, ensuring fertilization, cost-benefit analysis for how long
Mating in honeybees: during nuptial flight male and female mate
o Aedeagus: after mating the dying male disconnects, leaving
his aedeagus behind, this hinders a next mating, female must
remove it to oviposit, sperm storage can last for years
o Different genital apparatuses between bee species
War of the sexes
o Male: produce sperm, anti-aphrodisiacs, nutrients and/or toxins, sperm competition
 Taxonomy: male genitalia morphology
o Female: selects males, restrict access to spermatheca
o Traumatic insemination in bed bugs: male stabs female in abdomen to inject sperm, they provide their
sperm with antimicrobial compounds (lysozymes) to protect the sperm from mortality
Mating in Trichogramma parasitoids: males wait for females, perception of pheromone, immediate mating
Oviposition: some butterflies carefully glue their eggs to the leaf
o Egg care by adults: different species have methods, some beetles carry their eggs on their back
Larviposition: eggs hatch inside female, female lays of larvae (e.g. aphids)
Sex determination in insects: heteromorphic sex chromosomes, a lot of different systems
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Haplo-diploidy: haploid (n) males and diploid (2n) females, no
heteromorphic sex chromosomes, approximate;ly 20% of all
animals, evolved from paternal genome loss
o Sex determined in parasitoids: (n=male, 2n=female) females
always lay a combination of males and females, laying an egg
and keeping the spermatheca closed = son
o Special case: complementary sex determination: in diploids the alleles at the
sex locus determine sex  haploid = fertile male, homozygous diploid = not
fertile male, heterozygous diploid = female,  Single locus complementary sex
determination (SL-CSD)
 Diploid male costs: low survivorship, sterile
 Proportion of diploid males depends on: level of inbreeding inbreeding is punished severely,
level of polymorphism (number of sex alleles)
Genetic sex determination
o Sex chromosomes, haplo-diploidy, complementary sex determination
o Manipulators of sex determination in insects
 Cytoplasmic elements: microsporidia and bacteria (e.g. Wolbachia) in arthropods
 Nuclear elements: sex chromosome drivers in mammals, arthropods and plants, B chromosomes
in arthropods (e.g. PSR chromosome)
Wolbachia pipientis: α-Proteobacteria (Rickettsiae),
infects cell cytoplasm of insects (20-80%), vertically only
transmitted through eggs, cause cytoplasmic (spermegg) incompatibility, increase fecundity/fertility,
necessary for egg development, a lot of different things
in different species  manipulate sex determination
o Wolbachia-induced parthenogenesis: female
without mating produces fertile female offspring
 Parthenogenesis as an intrinsic phenomenon: aphids. Caused
by Wolbachia: parasitoids, thrips, ticks
o Can wasps get infected inside a host egg?  infected + not infected female lay eggs in host egg  all
individuals that hatch have Wolbachia  horizontally transmitted if feeding together in a host
o Male-killing by Wolbachia: -------------------------------------------------------------->
o Feminization by Wolbachia: -------------------------------------------------->
Sex ratio distorters: Wolbachia bacteria turns all offspring female and B
chromosome turns all offspring male
Wolbachia and B chromosome
o Trichogramma kaykai: 4-26% of females in field population infected with
Wolbachia, in other parasitoid species Wolbachia infection leads to
100% infection and elimination of sex  Why not in
Trichogramma kaykai?  B chromosome stabilizes
Wolbachia frequency by turning females into males
that cannot transmit Wolbachia
Summary
o Mate guarding to ensure paternity
o Costs of advertising for mates
o Mate selection for best options for offspring
o Provisioning partner for extra nutrients for offspring
o Genetic sex determination under complementary sex determination
o Sex determination and sexual reproduction can be manipulated by selfish elements
o Cytoplasmic Wolbachia bacteria manipulate sex determination and sexual reproduction in many
arthropod species
o Wolbachia can be frequently transmitted horizontally between and within species
o Horizontal transmission can contribute to spread within species
o B chromosome that eliminates paternal genome
Life History Evolution
Demography, selection and quantitative genetics
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Variation: why does it exist, how is it generated and how can it be used?
Natural selection: Historical influence of Darwin and Wallace, predictability of natural selection, natural selection
is associated with adaptations (general appeal)
o Adaptations: groups of traits
Life history: description of the traits of an organism, from conception to death ( life cycles)
o Principle life history traits: size at birth, growth pattern, age of maturity, size at maturity, age and sizespecific reproductive investments, number size and sex ratio of offspring, age and size specific mortality
schedules, length of life
o Shape of life histories are the result of natural selection, life histories considered central to the process of
adaptation, life history traits are principle components of fitness
Key aspects of adaptation: genetic tracking of environment through natural selection, phenotypic plasticity to
maintain fitness in new environment, genotype-by-environment interactions
Studying life history evolution: demography, quantative genetics, trade-offs and constraints
o Demography: age and size specific reproduction and mortality patterns allow for calculation of strength
of natural selection on life history traits under many different conditions
R-number: when > 1  population increasing, when < 1  more death than birth
if age-specific birth and death rates are constant in time and space  then population attains a stable age
distribution, ratios of individuals in different age classes remain constant
o Fitness is more sensitive to changes in mortality and fecundity in younger age classes than older
o Connection between fitness and evolution is direct: individual variation in survival and reproduction
causes variation in fitness and natural selection
Ageing as part of life history evolution: ageing is the total effect of those intrinsic changes that accumulate in the
course of life that negatively affect the vitality of the organism, and that makes it more susceptible to the factors
that can cause death
o Mortality: mtotal = menvironment +mintrinsic
o Decreasing me reveals ageing in humans as
well  when lowering me the curve of survival
goes up  better medical conditions in later
years so me is influenced
o Natural selection: maximal reproductive
output within the natural lifespan
o Ageing is non-adaptive and mechanisms evolved via two main routes:
 Private: unique, lack of selection for late-life fitness/health, no early life consequences,
accumulation of deleterious mutations with late life effects, contingency: private phenotypes and
mechanisms
 Public: shared, strong selection for early life fitness at expanse of late life health, late life
consequences, selection for genes with antagonistic pleiotropic effects, common principles: public
phenotypes and mechanisms
o Balance between reproduction and survival (more offspring, less
quality vs less offspring better quality) -------------------------------------->
o Age-specific natural survival patterns determine life history
Quantative genetics: focus on continuous phenotypic variation,
underpinned by multiple loci (polygenic inheritance), influenced by
environmental factors
o Three sources of variation: Genetic (G) variation, Environmental (E)
variation and G-by-E variation
o Genotype cannot be directly discerned by phenotype
o 𝑃 = 𝐺 + 𝐸 + 𝐺 ∗ 𝐸  Focus on continuous phenotypic variation
 𝑃 = phenotypic, 𝐺 = genetic, 𝐸 = environmental
o Majority of adaptive changes are smooth and involve Q-traits (Morphological, physiological, behavioural
and life history traits)
Quantify and track genetic variation over time and space  Partitioning phenotypic variation into its
underlying components:
 𝑃 = 𝐺 + 𝐸  𝑉𝑃 = 𝑉𝐺 + 𝑉𝐸 (variance)  𝑉𝑃 = 𝑉𝐴 + 𝑉𝐷 + 𝑉𝐼 + 𝑉𝐸
 𝐴 = additive, 𝐷 = dominance (interaction within loci), 𝐼 = interaction between loci
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Heritability (ℎ ): proportion of phenotypic variance (𝑉𝑃 ) that can be attributed to genetic variance (𝑉𝐺 )
o Measures phenotypic resemblance between relatives that share alleles
 Broad sense: 𝑯𝟐 = 𝑽𝑮 ⁄𝑽𝑷
 Narrow sense (determines evolutionary potential): 𝒉𝟐 = 𝑽𝑨 ⁄𝑽𝑷
o Estimating variance components by comparing resemblance between relatives
o Siblings share alleles and may share genotype / parents and offspring share alleles but not their genotype
How to measure heritability: parent-offspring regression
o If variation among individuals is due to variation in genes  offspring resemble parents
o Check this by plotting phenotype of offspring against parents  slope of regression line is the heritability
o Estimates narrow sense heritability ( part of genetic variation that is transmitted from parents to
offspring is used, and it’s “genotype independent” (parents and offspring share alleles but not same
genotype))
Estimating heritability: “Full-sib family analysis”
o 𝒉𝟐 = 𝟐𝝈𝟐𝒔 ⁄ (𝝈𝟐𝒔 + 𝝈𝟐𝒘 )
o Use ANOVA with family as factor  𝑀𝑆𝐸 estimates within family
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2
variance (𝜎𝑊
), 𝑀𝑆𝐵 estimates 𝜎𝑊
+ 𝑘 𝜎𝐵2
 𝜎𝐵2 = 𝜎𝑠2 = (𝑀𝑆𝐵 − 𝑀𝑆𝐸 )/𝑘, 𝑘 = number of full sibs
o Estimates broad sense heritability
o What variances does 𝜎𝐵2 = 𝜎𝑠2 contain?  sibs share on average ½
of alleles and in ¼ of cases has same genotype, thus the same
dominance deviation
 𝐶𝑜𝑣𝐹𝑆 = 𝜎𝑠2 = ½𝑉𝐴 + ¼𝑉𝐷
o A heritability estimate applies to: trait, population and environment under study
Heritability of a trait is not a constant  heritability of wing area in certain flies is present in higher latitudes
Heritability and fitness: why do life history traits have low h2?
o Life history traits closely related to fitness  experience strong natural selection  will deplete genetic
variation (𝑉𝐴 )  in addition, fitness traits especially sensitive to environmental influences (𝑉𝐸 higher)
Estimating the heritability from (artificial) selection experiments
o Breeders equation: response (𝑅) depends on selection differential (𝑆) and heritability h2  𝑅 = ℎ2 ∗ 𝑆
 Slope = h2 = [𝑂∗ − 𝑂̅]⁄[𝑃 ∗ − 𝑃̅ ] = 𝑅 ⁄𝑆
o Thus, you can calculate heritabilities from selection experiments (= realized h2)
o
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Life History Evolution
Phenotypic plasticity, trade-offs and constraints
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Phenotypic plasticity: the capacity of an organism to develop any of several phenotypic states, depending on
environment; usually this capacity is assumed to be adaptive
Bicyclus anynand has different strategies for different parts of the year
o Dry season: long lifespan, delayed reproduction, inactive behaviour, high fat content, cryptic wing pattern
o Wet season: short lifespan, fast reproduction, active behaviour, low fat content, conspicuous wing pattern
How are environmental signals translated into phenotypic traits?
o Residual metabolic rate drops + residual abdomen mass increases with increasing developmental temp.
o Hormonal regulation: ecdysone (steroid hormone, usually forms complex in cytoplasm  enters nucleus
 expresses certain genes), juvenile hormone (lipid hormone)
o Discrete hormonal dynamics correlates with discrete phenotypes that are likely related to fitness
Pupal hormone dynamics similar in shape across temps  developmental temp affects relative timing of
dynamics  dichotomy between lower vs higher temps
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Time point of injection of ecdysone in cold reared butterflies has a “window of sensitivity”  injection in this
window accelerates pupal development  cold reared butterfly looks like warm reared butterfly and has
relatively large abdomen
o “The results illustrate how organisms can use systemic hormones and their time- and tissue-specific sensitivity to
respond to predictive indicators of environmental quality and to make strategic life history decisions that enable them
to cope with fluctuating environments.”
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For plasticity to evolve you need genotype-environment interaction (G-by-E)  gives phenotypic variation 
selection for optimal genotype  𝑉𝑃 = 𝑉𝐺 + 𝑉𝐸 + 𝑽𝑮𝑬
Geographic variation: life history and wing pattern conclusions
o Population differentiation for wing pattern  Region-specific response, risk of phenotypic mismatch with
increasing temperatures associated with climate change
o Little differentiation for life history traits; no differentiation for traits that can acclimate during adult stage
 adult acclimation very important in coping with local climate
Trade-off: existence of both fitness benefit and cost of a mutation or character state, relative to another
Physiological trade-off: interrelated with micro-evolutionary, phenotypic plasticity
o Smith and Fretwell’s model on optimal size: optimal compromise between size and number of offspring
on good vs bad host  assume trade-off between size and number  above minimum size, probability
of survival increases with offspring size  minimal size for survival smaller on good host  parental fitness
is number of offspring multiplied by probability of survival  optimal offspring size bigger on poor host
 female can sense quality of host and adjust their reproductive output to that environment
Micro-evolutionary: often physiological for which there is genetic variation,
apparent in populations under natural selection, increase in one trait results
in decrease in another, include (most are) physiological trade-offs, genetic
variation present (maintenance of variation)
o Trade-offs and constraints visualised within time and space ---------->
o Genetics: antagonistic pleiotropy  genetic correlations between
traits predominantly negative (trade-offs)
 Pleiotropy: traits share similar genes that control their development or expression
 Allelic effects positively influencing both traits  fixed by natural selection
 Allelic effects negatively influencing both traits  removed by natural selection
 Allelic effects negatively influencing one, and positively the other trait  remain in population
o Physiological: resource acquisition and allocation
 Y-shaped model
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Linking physiology and genetics: what is the net effect of natural selection?
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r: regression coefficient
Food Webs and Multitrophic Interactions
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Community: group of interacting species
Assemblage: group of species on a particular resource without an assumption on their interactions
Component community: all species associated with a single resource (e.g. plant species)
Compound community: all species associated with all resources in community (e.g. plants in a habitat)
Food web: set of linkages among organisms in a community emphasizing feeding interactions
Food chain: chain of organisms linked together by being each others resource
Trophic level: a stage in the sequence of feeding interactions in a food web
o Bottom up: communities are shaped by composition (quality and quantity)
of lower trophic levels, cascading into effects on higher trophic levels
o Top down: communities are shaped by composition of higher trophic levels
that top down control the lower trophic levels
Compartmentalization: communities can be divided into separate trophic
networks that are independently affected by trophic processes
Connectance food web: food webs that shows all trophic links among species
Quantitative food web: shows relative sizes of populations in the food web
Within food webs important species characteristics are:
o Guild: group of species that exploit resource in similar way (such as phloem feeders, leaf chewers)
o Ecological niche: set of abiotic and biotic conditions in which a species can persist
 Evolution drives not to competitive exclusion  some form of coexistence/ niche behaviour
o Niche breadth: breadth of abiotic and biotic conditions in which a species can persist
!Genetic assembly rule: genetic distances between two plant genotypes  reflected in distance of dissimilarity
in insect community composition associated with the genotypes  plant genotype/characteristics determine
what kind of insect species are there
o The more genetic distance (difference in genotype)  the more insect assembly varies
o E.g. leaf shape and chemical composition of genotypes mediates effects in insect communities
Trophic cascades: effects of one trophic level are extended in effects on other trophic levels
Resource quality and quantity hypothesis: quantity and quality of a resource (plant) directly determines the
insect community composition
Plant traits that affect insect abundance:
o Size or biomass, leaf shape, leaf toughness, chemical composition, flower traits, etc.
Resource heterogeneity hypothesis: effects on herbivores  more diversity  more diversity herbivores 
more diversity natural enemies, increased heterogeneity, i.e. width of variation, results in more ecological niches
and thereby more diverse and species rich insect communities
Heterogeneity (variation in space) at different levels may cause similar effects:
o Variation in microclimate (abiotic effects), plant community richness, plant genotype richness, variation
in quality within a plant (old and young leaves, leaves and flowers, etc.)
o It matters who you are as an individual and it matters who’s around you in terms of species
Right or wrong neighbours: enhanced populations or decreased populations determined by who’s next to you
Resource-concentration hypothesis: concentration of resources determines insect community composition,
mono-cultures are likely to be colonized by specialists that have higher abundance than in mixed stands
Associational-resistance hypothesis: non-food plants interfere with location of food plants for specialist
herbivores, thereby specialists are less abundant in mixed stands
Associational-susceptibility hypothesis: attractive neighbouring food plant may cause higher colonization of
focal plant by herbivores
Enemy-impact hypothesis (or top-down regulation of communities): rich plant communities sustain large
predator communities (due to food availability and niche richness) that regulate herbivore communities
o Plant traits may directly influence interactions with predators, the enemy of your enemy is your friend
 Resource mediated indirect resistance: food, shelter  acacia species has extrafloral nectaries
which attract ants that guard the plant  using something for its own benefit  indirect
 Information mediated indirect resistance: herbivore induced plant volatiles that attract natural
enemies  plant accessions (cultivars/genotypes) differ in volatile production after herbivory 
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attractive plant accessions harbour more parasitized caterpillars  attractiveness attracts natural
enemies of plants natural enemies
o Interactions over four trophic levels: the enemy of your enemies enemy  hyperparasitoids how do they
find a host?  plant volatiles induced by parasitized herbivores  parasitoid changes herbivore
environment  difference in regurgitate of caterpillar  plant excretes different volatiles
Parasitism: polydnavirus, venom and eggs
o Parasitoid (C. glomerata) carries own virus, use that to supress immune
of caterpillar  in genome of parasitoid is genome of virus  own benefit
 less encapsulation of eggs by caterpillar ( maybe Hypersoter has a
benefit of this virus as well since in practical you can see there was more
encapsulation with the solitary parasitism than when multiparasitised) 
venom helps virus in changing herbivore
Symbiotic virus reveals parasitoid to its enemies  removing salivary gland of
caterpillar knocks out the whole interaction and hyperparasotoid cannot
distinguish parasitised from unparasitized
Summary:
o Insect communities are strongly shaped by plant traits
o Genotype assembly rule very important, also GAR vs heterogeneity
o Resource quality and quantity hypothesis: trophic cascades by plant quality shape herbivore and
predator communities
o Resource heterogeneity hypothesis: species and genetic plant diversity positively affects insect
communities by niche richness
o Resource concentration hypothesis: Monocultures promote specialist abundance
o Enemy-impact hypothesis (multi-trophic interactions): Insect communities are also top-down regulated
and plant traits may directly affect abundance of predators promoting top-down control
Community Ecology
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Temporal effects (not all members of food web are there at the same time) have consequences on structure of
an insect community  removing one species from food web has drastic consequences  secondary extinctions
in simple webs  more stability in complex webs  food web complexity reduces extinction cascades
Indirect plant-mediated species interaction: many plant species respond to insect attack instead of having
defences up all the time (too much cost)  plant recognises insect saliva and has a specific attack to specific
insects  consequences: responding to one herbivore makes it so that other herbivores don’t find plant in
normal state but in induced state  this could interfere with insect choices  positive (herbivore wants induced
plant) or negative (herbivore leaves plant alone)  matters who is coming first, second, etc.  all interconnected
Trait mediated interaction unit (TMIU): initiator alters trait in shared resource (plant)  effect on receiver
Indirect trait mediated response across trophic levels: induction by herbivory leads to altered volatile emission
that is used by parasitoids to locate herbivore
Important aspects of trait mediated effects in insect communities: insect species induce specific responses in
plant, vary in scope of affecting plant phenotypes as sequential herbivore, vary in temporal effect size on plant
phenotypes, differ in response level and direction to previous damage
Genotype by inducer interaction: specificity of induction for plant genotypes
Some plants play with insect interactions  tobacco plant is stripped by hornworm and really doesn’t want this
 mired bugs do a little damage but not much  hornworms are less frequent in plants infected with mirid bugs
 plant attracts mirid bugs to avoid hornworms
Specificity in plant-mediated herbivore interactions: interactions between herbivores are asymmetric,
interactions may be specific for genotypes, plant physiology drives specificity in interactions among species
Plant physiology drives specificity in interactions among species
o Feeding guild: sap sucking vs leaf chewing induce different hormone pathways in plants, feeding pattern:
amount and pattern of damage induces different responses, herbivore specific elicitors: each herbivore
species has a different mix of elicitors in their saliva
o Also above-belowground interactions: plant moves energy to roots if roots are attacked  leaves more
susceptible  vice versa
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Herbivore pollinator effects: flowers respond to damage on leaves, physiology of flowers change  less visits of
pollinators if affected by herbivore  very specific responses  different herbivore has different effects on
flowers  pollinators affected by how much plant is affected  more damage  less pollinators
Herbivore community wide effects: arrival of one herbivore changes entire community on said plant
Genotype effects overridden by phenotype effects done by herbivores  predictable responses in community
Specialised herbivores pick up plant volatiles plant puts out to avoid predation  plant easier to find
Herbivore community wide effects:
o Induced responses link species that are not trophically linked
o Early season herbivores may shape composition of insect communities
o Not all herbivores have plant mediated effects + insect species differ in responsiveness to induced plants
o Effects of early season herbivores may be larger than effects by plant genotypes
Interaction networks: series of trait mediated interaction units (e.g. receiver is inducer to next receiver)
Predator mediated effects (consumptive and non-consumptive):
o Consumptive: trophic actual eating of herbivore,
o Non-consumptive: ecology of fear, predator being present changes behaviour of herbivore and has other
effects on herbivore (fleeing, eating in different pattern, etc.)
Aphid and ant mediated effects: aphids induce changes in plant quality
affecting herbivore colonization  ants feeding on sugars of aphids
reduce herbivore load on plant  dominant effect on herbivores on
plant
Parasitoid mediated effects: parasitoid is initiator  herbivore
physiology changes (initiator)  plant affected differently  different effects on other species (receivers)
o Quantitative differences in leaf tissue removed by parasitized herbivores
o Presence of parasitoids has a big effect on which genes are expressed
by plant  who is inside herbivore strongly effects responses in
plants  salivary aspect is most important for plant reactions
(parasitoid present has other compounds in saliva than parasitoid not
present)
o  Parasitoid strongly influence plant responses, each species
of parasitoid may have a different effect on plant, subsequent
colonization by other herbivores, parasitoids or
hyperparasitoids is affected by parasitism
Spatial aspects in community dynamics by trait mediated interactions
o Herbivores interconnect communities on different plants ---->
o Aphids usually feed on flowers  flowers have certain caterpillar
 aphids move to leaves  has effect on caterpillar that normally
feeds on leaves  behavioural change
o Predator mediated spatial processes: caterpillar moves from
plant a to plant b when parasitoid present on plant a  has
effect on caterpillars on plant b ------------------------------->
Be able to illustrate the complex interactions
Insect communities are organized by trait mediated interaction webs
o Specificity of plant responses to insect attack
o Physiological interactions within plants
o Temporal chain reaction of indirect effects
o Spatial chain reaction of indirect effects
o Ecological consequences for herbivore diversity
o Trophic structures comprise feedback loops that form an important indirect interaction web that
structure insect communities in addition to trophic processes
Individual plant is interacting with an individual subset of herbivores  plants know: when a was there, then d
and e won’t be because they don’t like it  plant anticipates on a, b and c and can predict community processes
 some respond very strongly to first herbivore  some don’t respond strongly because they take other
herbivores (that may be worse) in the long run into account
Ecological Genetics and Evolutionary Ecology
Spatially structured populations, detection selection: population genomics, geographic mosaic of co-evolution,
application to model system
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Central issues
o Genetics underlying natural adaptations: role of major genes, role of epistasis (gene interaction)
o Role of space in selection: spatial heterogeneity may influence evolutionary trajectory
Panmictic population: random mating, where all individuals are potential partners, assumes no mating
restrictions, neither genetic nor behavioural  no structure
Structured population: sub-populations connected by migration or dispersal
Genetic drift: change in allele frequencies due to random processes
Measure to express extent of population structure, using neutral markers: 𝐹𝑠𝑡 = ( 𝐻𝑡 − 𝐻𝑠 ) / 𝐻𝑡
o Neutral marker: doesn’t have any advantage or disadvantage  no selection
o 𝐻𝑡 : expected heterozygosity whole population
o 𝐻𝑠 : expected heterozygosity sub-populations (weighted average corrected for subpopulation size and
allelic frequency)
o 𝐹𝑠𝑡 varies between 0 (no population structure) and 1 (subpopulations fixed for alternative alleles)
Microsatellite: DNA sequence that is in the junk DNA, repeated a number of times units of a particular order,
due to errors by DNA-polymerase  e.g. 21 copies is one allele of a neutral marker
Example neutral loci: allozymes: variant forms of an enzyme which differ structurally but not functionally from
other allozymes coded for by different alleles at the same locus  not under selection
Redefinition population structures:
o Panmictic population: neutral alleles show no difference between samples
o Sub-populations connected by migration: samples may differ in neutral allele frequencies, and
heterozygosities in subpopulations lower than expected
 Disentangle effect of migration vs selection on allele frequencies at adaptive loci  genome-wide
vs. locus-specific effects (e.g. migration, genetic drift [including founder effects, bottlenecks],
inbreeding and selection, mutation, recombination, assortative mating)
Population genomics: compare population-level measure of genetic variability for locus of interest with
distribution of this measure for a large number of neutral loci
o E.g. 𝐹𝑠𝑡 : genome wide effects are influenced by chance  particular distribution of values for 𝐹𝑠𝑡 for
different neutral loci  locus specific effects will lead to 𝐹𝑠𝑡 in the tails of distribution
o If you make an 𝐹𝑠𝑡 distribution for neutral markers and compare this to other alleles  if very similar then
there is (almost) no selection on the allele of interest (since no selection on neutral markers)
Two possible applications:
o Generate candidates for loci that may be under selection
o If candidate loci already exist, make inferences on processes responsible for distribution of alleles at these
loci
Coevolution: reciprocal evolutionary response between members of different species, spatially structured
Geographic mosaic of coevolution: geographic selection mosaics, trait remixing, coevolutionary cold- and hot
spots  How can we identify coevolutionary hotspots?  population genomics:
E.g. interaction between flea beetle Phyllotreta nemorum and its host plants
o Polymorphism in ability of P. nemorum to use defended plant Barbarea vulgaris (triterpenoid saponin) as
host and polymorphism in Barbarea vulgaris in chemical defence  larvae collected on Barbarea: 100%
resistant  larvae collected on other plants low % resistance
o Why are resistant P. nemorum rare on other plants?  1. Local adaptation and migration limited or 2.
Local adaptation and selection against migrants  for population genomics needed: neutral markers and
candidate locus adaptation
o Conclusion: discrete classes of phenotype (larval survival on Barbarea) show that major genes play a role
 identify these genes: candidate gene approach
o Migration: seems slightly limited between plant patches due to geographic distance
o  combine genetic data with neutral markers (population genomics)
What could selection involve?  R-genes appeared to have no negative effects when beetles use other
host plants, but: homozygous beetles have high mortality after backcrossing with susceptible line; also
after outcrossing with susceptible field-population?
 R-gene has a negative effect on fitness (if homozygous) however
compensatory genes negative effect on R-gene and thus having a
positive effect on fitness
 Thus  selection against resistant migrants that migrated to other
plants than Barbarea  through break-up of co-adapted gene complexes (?)
Other factors influencing distribution of resistance genes
o Abundance and distribution of host plants (asymmetric gene flow)
o Host plant phenology
o Variability in host plant defence
o Parasitism/predation
o Other interactions, e.g. with fungi
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Insect Ecology, Invasion Biology and Climate Change
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Climate change:
o Move (habitat tracking)  may lead to invasion
o Change phenotypically (phenotypic plasticity)
o Adapt genetically
o Effects expected in insects because of ectothermic (poikilothermic: internal temp varies) character
Reaction norms: characterizes phenotypic plasticity by describing how target phenotype for specific genotype
varies as a function of an environmental variable  may be under selection because of climate change
How can one study influence of climate on insects? 
spatial and temporal observations/monitoring
Cline: gradual change in character or allele frequency along
geographic transect, gradual vs stepped shape, originate
by: interbreeding between formerly isolated populations,
geographic variation in selection pressure
o Can occur: in continuous environmental gradients,
when selection favours different genotypes in
discrete environments, similarly when environment
changes more gradually, shape also depends on
gene flow
Clinal variation e.g.: melanism in Adalia bipunctata  correlation of melanism clines and climatic factors
o Hypothesis: thermal melanism  melanic individuals have advantage relative to non-melanics under
particular climate conditions, due to more efficient absorption of solar radiation caused by dark coloration
of their surface  differences in climate lead to geographical variation in fitness of morphs, and thus to
clines in morph frequencies
o Testing: interdisciplinary approach involving biophysics, behaviour and population genetics  melanics
reach a higher body temperature  quicker active and walk faster
o Results: geographic variation in melanism (clines), correlation %-melanics vs climate, higher body temp
and activity of melanics in lab, higher activity of melanics in field, clines are changing, correlation changing
clines with climate change  climatic actors influence melanism in Adalia bipunctata
Above example of morphological adaptation. Other consequences of climate:
o Phenology: on life-history traits
o Synchrony: on species interactions
o On dispersal/migration  invasion
Possible reasons for disproportional success of invaders:
o Release from natural enemies
o Entering of ovel niche with less competition than in original area
Characteristics of successful invaders: generalist/polyphagous, low habitat specificity, high fecundity (natural
capability to produce offspring), large body size, high dispersal ability
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Invasive species: introduced by human action where it did not previously occur naturally, capable of establishing
breeding population without further invention by humans, becomes pest, threatening agriculture/local
biodiversity, “invasive species” refers to subset of species defined as “introduced species”
o Introduction by: rapid climate change, accidental hitch-hiking, intentional release
Impact of invasive insects:
o Genetic: hybridization or introgression (transfer of genetic material from one species into gene pool of
another by repeated backcrossing of an interspecific hybrid with one of its parent species)
o Individual: changes in morphology, behaviour, demography
o Population: structure, abundance or dynamics of native species
o Community: resulting from population impacts
o Ecosystem: changes succession, decomposition, nutrient cycleing
o Landscape, regional and global impacts