ICA 3 PREDATION
GROUP ______________________
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ADAPTATIONS OF PREDATOR AND PREY
1. What adaptations allow predators to catch/process prey?
bigger size, faster speed, methods to capture/kill/process prey, even if prey is bigger
than predator.
2. What adaptations allow prey to avoid predation?
1. group living 2. induced structureal defense 3. chemical defense
4. cryptic coloration 5. aposematism
6. mimicry of unpalatable species
3. Figure 1A/B Why does group living deter predation?
Increases distance predator first seen; lowers probability of being attacked.
4. Figure 2A. How can the ‘induced defense hypothesis’ be tested?
Compare thickness of shell when mussels are grown in sea water with and without
their predator, the crab.
Figure 2B. What is the independent variable? presence/absence of predator
What is the control treatment? sea water without predator
Figure 2C. What is the conclusion? predator induces structural defense of prey
5. Figure 3. What prey trait must accompany its aposematism to deter predators?
toxin that makes them unpalatable to predator
What must the predator do to make it work for the prey? Predator must eat a
toxic prey and learn from its mistake so that it eats no more of this prey type.
6. Figure 4. In Batesian mimicry, is the model or mimic palatable? mimic
Which must be more common: model or mimic? model Why? predator must
have greater chance of encountering unpalatable model so that it learns to
avoid any organism with this color pattern, including the mimic.
7. Figure 5. How do Batesian and Mullerian mimicry differ? Batesian: one unpalatable
model and one palatable mimic; Mullerian: multiple species unpalatable
How many species are palatable? 0 unpalatable? all in Mullerian mimicry?
How does it deter predators? More species with same morphology/color increases
probability that predator encounters at least 1 prey; all species benefit from that
one species.
HOW TEST IF PREDATORS CONTROL PREY?
8. Figure 6. Do predators control predator abundance?
If….predators control predator abundance,
then….prey populations will be greater when predator is removed relative
to prey population with predator present.
Do skunks control duck populations? yes
9. Figure 7. What trait of predators might explain this predator’s response to prey
abundance? Territoriality; they don’t shrink area of dominance and let in more owls.
RESPONSES OF PREDATORS TO PREY DENSITY
10. Figure 8. What do functional response curves summarize?
Which variable is independent? prey density dependent? # prey eaten
Describe each response curve type.
I. Prey capture is directly proportion to prey density.
II. Prey capture increases, but then levels off at high prey density
What accounts for the shape of this curve? Predator gets full = satiated
III As type II, but prey capture is also low at low prey density.
What accounts for the left hand part of this sigmoid curve?
1. heterogeneous habitat; prey has hiding places
2. lack of learned search behavior by predator
3. predator switches to alternative prey at low prey density
Are these curves describing individual or population responses? Individual
What type of curve? kestrel I moose II
mayfly III
Figure 9. What type of response results from switching to alternative prey when
preferred prey become scarce? III
11. Figure 10. What is meant by a ‘numerical response of predators? Changes in
predator population size by increased birth or decreased death rates – or by
immigration when prey populations increase.
Is it an individual- or population-level response? population
12. Figure 11. Moose-wolf What type of response? numerical
Describe the pattern. As moose density increases, wolf density increases and then
appears to be leveling off.
Speculate why a ‘leveling’ to a stable level occurs for wolf density. Wolf packs
have maximum density to be functional; can’t expand infinitely.
13. Figure 12. Warblers and budworms
A. What is independent # prey dependent variable? #prey per gizzard (of individual)
Functional or numeric response? functional type? II
B. What is dependent variable? # nesting pairs of birds
Functional or numeric response? numeric Describe the curve. Concave.
Increases with increasing prey density, but at lower rates at higher densities.
C. What is the dependent variable? % mortality due to predation.
Describe the pattern. Increases only at low prey density but then steadily
falls as number of prey increases.
Does the warbler population control its prep population? No. Explain
why there has been widespread damage by this insect. Individual birds get
satiated at low prey densities; bird population size does not respond linearly to
increasing prey density. As a result the prey population explodes without
adequate predator control.
PREDATOR-PREY CYCLES
14. Figure 13 + 14. What is meant by synchronized All species population cycles rise
and fall at the same time vs. asynchronized cycles? Species population cycles rise and
fall at different times.
15. Figure 15. In these cycles, which group lags the other? predator lags prey Why?
Prey must increase first before predators can increase birth rate (or decrease death
rate).
What are two factors that could explain the cycle of prey?
Abundance of predator
Abundance of food
Figure 16. What is different in this hypothesis from all previous hypotheses of the
semester? Two, not one, independent variable.
What are the two independent variables? predation; food availability
How many treatments must be in this experimental design? 4 Name them.
normal predator/food (control); no predator; added food; both no predator/add food
What is the dependent variable? prey density
Figure 17. What is the conclusion? Prey density is strongly increased when predators
are absent and added food is given; other variables similar to control.
What would have been the conclusion if each independent variable had been tested
separately? Neither predator or food availability are very important in control
prey denstiy
What is the ‘take-home’ message? Ecology is complex! Simple experiments testing
only one variable may lead to misleading results. Assumptions (e.g. food is plentiful)
may also need to be tested at the same time as the principal variable (predator).
16. Figure 18. In a measles epidemic who is the predator? measles virus prey? humans
Which lags which? virus lags behind buildup of non-immune prey. Explain how the
cycles ‘work’. Non-immune humans increase  virus increases.
Non-immune humans fall; most have gotten virus + are immune  virus decreases.
New children born with non-immunity  virus increases again.
Why does data collection stop in 1970? Vaccinations brought immunity so measles
cases stopped.
17. Figure 19. Gause’s experiments
A. Is the cycle stable? no Explain what is happening. Prey increases, but predator
increases sufficiently to wipe out prey population. No cycle.
B. What factor allowed prey to thrive? presence of hidey holes (refuges)
C. What factor allowed the cycles to stabilize? immigration of prey from other
subpopulations.
18. Figure 20. Huffaker’s experiments
What was the response of the predator-prey cycles if:
A. oranges clumped and no immigration possible No stability.
B. oranges dispersed randomly (+ vasoline prevented predator movement, while
pegs allowed prey to parachute to new locations) Stability
What is meant by spatial heterogeneity? Variability in the environment
19. Summarize. What factors enhance stability of predator-prey cycles?
1. places for prey to hide from predator
2. immigration of prey from source subpopulations
3. spatial heterogeneity so predator has to work harder to find scarce prey