Control and coordination
AL Bio
The endocrine system
• A hormone is a chemical substance, produced by an endocrine gland and
carried by the blood, which alters the activity of one or more specific target
organs
• Hormones are used to control functions that do not need instant responses
• Hormones are produced by endocrine glands
• The endocrine glands that produce hormones in animals are collectively
known as the endocrine system
• A gland is a group of cells that produces and releases one or more
substances (a process known as secretion)
• The glands contain capillary networks and specialised secretory cells that
make and release hormones.
Features of the endocrine system
• Hormones are released from the cells of the ductless gland, directly into the blood
stream
• Hormones are then transported in blood to the target organs
• Cells of the target organ possess specific receptor molecules on the external surface of
their cell surface membrane
• The hormone molecules binds to the specific receptor sites on the cell surface
membrane of target organs
• Receptors are complementary to the specific hormone
• Hormones such as insulin, glucagon and ADH are cell-signalling molecules that are
released into the blood. They are carried in blood to target organs.
• These hormones bind to receptors on the cell surface membranes of their target cells.
• This activates second messengers to transfer the signal throughout the cytoplasm
• These hormones are water-soluble and so cannot cross the phospholipid bilayer of cell
surface membranes. Some hormones are lipid soluble and cross the phospholipid bilayer.
These bind to receptors in cytoplasm or nucleus of target cell e.g. testosterone
Comparison of the nervous system and the endocrine
system - differences
Comparison of the nervous system and the
endocrine system - Similarities
Sensory neurone
• Transmits impulses from the receptors to the CNS (brain or spinal cord)
• The cell body is found in the dorsal root ganglion which is a swelling of the spinal cord . Has a
nucleus in the cell body
• Has many mitochondria in the cell body
• Many RER /ribosomes/presence of Nissl’s granules in the cell body
• Have a long dendron in cell body which transmits impulses to the cell body. Dendrites are
attached to the dendron
• Have a short axon which carries impulses away from the cell body
• The axon is insulated by a fatty sheath called the myelin sheath.
• The myelin sheath is made by specialised cells known as Schwann cells
• Myelin is made when Schwann cells wrap themselves around the axon along its length
• Between Schwann cells are gaps of unmyelinated axon regions called Nodes of Ranvier .The
electrical impulse does not travel down the whole axon, but jumps from one node to the next by
saltatory conduction
• Nerve axon is expanded (swollen) at the end to form a bulbous ending called the axon terminal
or synaptic knob
Sensory Neurone
Motor neurone
• Motor neurones transmit impulses from CNS to effectors (muscles/glands)
• They have a cell body at one end. The cell body is found in the CNS
• The dendrites lead to cell body
• They have a nucleus in the , cell body / soma
• They have many mitochondria in cell body
• They got much RER / Nissl’s granules in cell body
• They have one long axon
• The synaptic, knobs / termini / boutons are at end furthest from cell body
• The have Schwann cells which produces myelin sheath an insulator of the
axon
• Unmyelinated regions of the axon are called Nodes of Ranvier
A motor neurone
Intermediate neurones
• Intermediate neurones connect sensory neurones and motor
neurones
Contrast the structure and function of sensory
neurones and motor neurones
Myelin sheath and the Schwann cells
Sensory receptors
• Sensory receptors are receptor cells that detect and respond to chemical stimuli.
• Examples of chemical stimuli are light, heat, sound, touch, pain, chemicals, taste and smell
• Sensory receptors act as transducers i.e. convert stimulus energy to electrical energy
• This a produces generator / receptor potential
• The sensory receptors passes the impulse, to the sensory neurone
• Some sensory receptors are found in taste buds on the tongue
• The surface of the tongue is covered in many small bumps known as papillae.
• The surface of each papilla is covered in many taste buds
• Each taste bud contains many receptor cells known as chemoreceptors.
• These chemoreceptors are sensitive to chemicals in food and drinks
• Each chemoreceptor is covered with receptor proteins
• Different receptor proteins detect different chemicals
Role of sensory receptor cells in detecting stimuli and
stimulating the transmission of impulses in sensory neurones
• The chemicals act as a stimulus
• The chemoreceptors are specific for different chemical
• Sodium ions diffuse into the chemoreceptor cell through microvilli
• This leads to depolarisation of the chemoreceptor cell membrane
• This generates a receptor potential / generator potential where there is an increase in
positive charges inside the cell
• The receptor potential stimulates the opening of the voltage gated calcium ion channels
• Calcium ions enter the cytoplasm of the chemoreceptor cell
• This causes movement of vesicles containing neurotransmitter from the basal membrane
of the cell
• The neurotransmitter is released by exocytosis
• The neurotransmitter stimulates an action potential (impulse) in the sensory neurone
• The chemoreceptors are transducers
Role of sensory receptor cells in detecting stimuli and stimulating the
transmission of impulses in sensory neurones (contnd)
• A stimulus must be at or above a minimum intensity, known as the
threshold of stimulation, in order to initiate an action potential
• If the stimulus is below the threshold of stimulation, the receptor
cells will not be sufficiently depolarised and the sensory neurone will
not be activated to send impulses
• If the stimulus is strong enough to increase the receptor potential
above the threshold potential then the receptor will stimulate the
sensory neurone to send impulses
• This is an all-or-nothing principle
All or nothing law
Note : As the strength of stimulus increases beyond the threshold , the frequency (not
amplitude) of action potential increases
Generation of an action potential in a sensory neurone,
using a chemoreceptor cell in a human taste bud as an
example
• Chemoreceptors in the taste buds that detect salt (sodium chloride) respond directly to sodium
ions in food. When food containing salt is eaten:
• Na+ ions enter the chemoreceptor cell through channel proteins
• The cell surface membrane of the chemoreceptor cell is depolarised
• This generates receptor potential if the stimulus is above threshold
• Voltage-gated calcium channels open
• Ca2+ ions enter the cytoplasm of the chemoreceptor cell
• Vesicles containing the neurotransmitter move towards and fuse with, cell surface
membrane ( presynaptic membrane )
• This causes exocytosis of the neurotransmitter
• The neurotransmitter binds to receptor on, postsynaptic membrane / sensory neurone
• Sodium ion channels open and Na+ enter the sensory neurone
• The postsynaptic membrane / sensory neurone membrane is depolarised
• An action potential is generated if the stimulus is above threshold.
Voltage - gated channels
• These are trans- membrane proteins that transports ions
• They open / close when, voltage / depolarisation / charge / electrical
potential, changes
• Voltage -gated channels are specific to the ion that they transport
• Have a hydrophilic pore
Transmission of nerve impulses in a myelinated
neurone
• Resting potential
• Action potential
• Refractory period
Resting potential
• In a resting axon the inside of the axon always has a slightly negative electrical potential compared to the
outside of the axon
• This potential difference is usually about -70mV
• This is called the resting potential and in this condition of the inside of the axon is said to be polarised.
• Axon phospholipid bilayer is impermeable to K+/Na+
• Na+/K+ pumps are in the cell surface membrane. Na+ move out of the axon K+ enter the axon by active
transport. This uses ATP
• Three Na+ move out of the axon for every two K+ that enter the axon
• Some K+ diffuses out of neurone and Na+ diffuses into the cell by facilitated diffusion through protein
channels
• More K+ diffuses out than Na+ diffuses in. This is because the membrane is more permeable to K+ than Na+
• The inside of, axon / neurone, is more negative (than outside).Membrane /cell is repolarised
• Resting potential is -70mV. K+ are responsible for resting potential
• Ion movement occurs only at the Nodes of Ranvier
• The voltage gated channels are closed during the resting potential
Resting potential
Transmission of an action potential in a
myelinated neurone
• An action potential is a temporary, local reversal of the potential difference from a negative
charge (- 70mV) to a positive charge (+ 40mV) when the axon is stimulated
• The Na+ voltage gated channel proteins open increasing permeability of membrane to Na+
• Na+ enters axon through facilitated diffusion. This causes depolarisation
• The potential difference inside the axon becomes positive at + 40 mV
• After 1 ms after an action potential in a section of axon membrane is generated, all the Na+
channels close. Na+ diffusion into the axon stops.
• K+ channels open. K+ moves out of the axon . Repolarisation occurs. The potential difference
becomes negative
• There is a short period of hyperpolarisation. This is when the potential difference across this
section of axon membrane briefly becomes more negative than the normal resting potential
• This is caused by delay in the closure of K+ channels resulting in more potassium ions leaving the
cell leading to a more negative potential difference
Transmission of an action potential in a
myelinated neurone (cont)
• The K+ voltage-gated channel proteins then close. The Na+ channel proteins in this section of membrane
become responsive to depolarisation again
• For a brief period, following the passage of an action potential, the neurone fibre is not excitable. This is
called the refractory period. This is due to an excess Na+ inside the axon
• As the K+ channels close, Na+ channels open and Na+ leave the axon. The neurone becomes responsive to
action potentials again.
• The depolarisation of the membrane at the site of the first action potential causes current to flow to the
next section of the axon membrane, depolarising it and causing Na+ channel proteins to open
• Localised electrical circuits are established
• Myelin (sheath) / Schwann cells, insulate the axon and prevent ion movement in these regions of the axon
• Action potential/depolarisation occurs only at nodes of Ranvier
• Action potential moves by saltatory conduction as it jumps from node to node enabling fast transmission
• Transmission of action potential is one-way / unidirectional
How the resting potential is restored during the refractory
period
• After 1 ms after an action potential in a section of axon membrane is generated, all the Na+ channel proteins
close
• This stops Na+ diffusing into the axon
• At the same time K+ channel this section of axon membrane now open. K+ ions diffuse out of the axon
• This returns the potential difference to normal -70 mV in a process known as repolarisation
• There is actually a short period of hyperpolarisation.
• This is when the potential difference across this section of axon membrane briefly becomes more negative
than the normal resting potential
• This is caused by delay in the closure of K+ channels resulting in more K+ leaving leading to a more negative
potential difference
• The K+ channels then close and the Na+ in this section of membrane become responsive to depolarisation
again
• Until this occurs, this section of the axon membrane is in a period of recovery and is unresponsive.
• This is known as the refractory period
• The Na+/K+ pump continues to pump Na+ out and K+ in and this helps to maintain the distribution of Na+ and
K+ across the membrane so that more action potentials can occur
The refractory period starts when repolarisation starts and finishes when resting state is established
Rapid transmission of an impulse in a
myelinated neurone
• Myelin sheath is an insulator / ions cannot pass through it
• depolarisation / action potentials, occur at nodes of Ranvier only)
• Therefore there are longer local, circuits / currents
• Action potential jumps from node to node through saltatory
conduction
• This makes transmission / conduction, faster
• In unmyelinated neurones, the speed of conduction is slow, being as
low as 0.5 ms−1 in some cases. In a myelinated human neurone,
action potentials travel at speeds of up to 100 ms−1
Saltatory conduction
Diameter of neurone and speed of conduction
• The speed of conduction of an impulse along neurones with thicker axons is
greater than along those with thinner ones
• Thicker axons have an axon membrane with a greater surface area over which
diffusion of ions can occur
• This increases the rate of diffusion of Na+ and K+, which in turn increases the rate
at which depolarisation and action potentials can occur
• Speed of transmission of the action potential along the axon membrane depends
on the resistance offered by the axoplasm within
• This resistance is related to the diameter of the axon
• The narrower the axon the greater is its resistance and the lower the velocity of
conduction of action potential.
• The larger the diameter of the axon, the faster action potentials are conducted.
The importance of the refractory period in
determining the frequency of impulses
• It controls maximum frequency of action potentials. Ensures that
action potentials are separate events stopping them from merging
into one another
• It ensures the impulse can only travel in one direction
(unidirectional). Nerve impulses only pass in one direction from active
to resting region. This is because the previously active region
undergoes a recovery phase during which the axon membrane cannot
respond to depolarisation even if stimulus intensity is increased.
Speed of transmission in a myelinated and unmyelinated axons of
different diameters
The structure of a cholinergic synapse
• A synapse is a junction between two neurones
• At the synapse the nerve axon is expanded (swollen) to form a bulbous
ending called the axon terminal or synaptic knob
• The synaptic knob lies in close proximity to the membrane of the dendrite
• The neurone immediately before the synapse is the presynaptic neurone
and is bounded by the presynaptic membrane
• The neurone after the synapse is the postsynaptic neurone and is bound by
the post synaptic membrane which is also thickened
• The presynaptic membrane is modified for attachment of synaptic vesicles
and release of transmitter substance into the cleft
The structure of a cholinergic synapse (cont)
• The post synaptic membrane possesses a number of large protein
molecules which act as receptor sites for acetylcholine
• The gap between the two membranes is called a synaptic cleft. The
synaptic cleft is 20nm wide
• The cytoplasm of the synaptic knob contains many mitochondria,
microfilaments and structures called synaptic vesicles
• Each synaptic vesicle has a diameter of 50 nm and contain a
neurotransmitter substance called acetylcholine
• Acetylcholine is responsible for transmission of nerve impulse across the
synapse
• The neurones that contain and release acetylcholine are known as
cholinergic neurones.
Transmission of impulse across a cholinergic
synapse
• An action potential reaches the presynaptic membrane
• Ca2+ channels open in the pre-synaptic membrane
• This increases the permeability of the pre-synaptic membrane to Ca2+
• Ca2+ enters pre-synaptic neurone by facilitated diffusion
• This causes the vesicles with acetylcholine to move towards and fuse with the pre-synaptic
membrane
• Acetylcholine is released by exocytosis
• Acetylcholine diffuses across synaptic cleft and binds to receptors on post-synaptic membrane
• Ligand-gated Na+ channels open and Na+ enters the post-synaptic neurone
• An action potential is generated in the post synaptic neurone
• Acetylcholinesterase, breaks down acetylcholine into acetate and choline
• This prevents the sodium ion channels staying permanently open and stops permanent
depolarisation of the postsynaptic membrane
Transmission of an impulse across a cholinergic synapse
Role of acetylcholinesterase in a synapse
• Acetylcholinesterase breaks down acetylcholine, so that
acetylcholine leaves the receptors in the postsynaptic membrane
• This stops depolarisation in the postsynaptic membrane
• It stops continuous action potentials in postsynaptic membrane
• Acetylcholine is recycled in presynaptic neurone
Effects of drugs on the synapse
• Drugs can affect synaptic transmission
• Some drugs have same shape as neurotransmitters.
• These drugs mimic the action of neurotransmitters at receptors
• This means more receptors are activated
Effects of drugs on the synapse
• Some drugs block the receptor molecules at neuromuscular junctions
• This stops the acetylcholine from binding to the receptors on the
post synaptic membrane
• This prevents the opening of voltage gated sodium ion channels
• Na+ do not diffuse into the post synaptic neurone. No or less
depolarisation
• This means action potentials are not generated
• This results in muscle paralysis
Effects of drugs on the synapse
• Some drugs inhibit the release of neurotransmitters from the
presynaptic neurone
• So there is no / less, binding of acetylcholine to receptors in the post
synaptic membrane
• The voltage- gated sodium channels remain closed
• No diffusion of Na+ into the post synaptic neurones
• No action potentials generated
Effects of drugs on synapses
• Some drugs inhibit the enzyme acetylcholinesterase on the post
synaptic membrane
• This means that acetylcholinesterase / Ach, remains attached to
receptors on post-synaptic membrane
• Voltage-gated sodium ion channels remain open
• Na+ continues to diffuse into post-synaptic neurone
• The postsynaptic membrane remains depolarised / repolarisation of
postsynaptic membrane does not occur
• Therefore there is continuous transmission of action potentials
Roles of synapses in the nervous system
• Ensure one-way transmission of impulses as receptor proteins are
only in the postsynaptic membrane
• Allows interconnection of nerve pathways since the post-synaptic
neurone may receive action potentials from different types of
neurones giving a wide range of responses
• Involved in memory / learning due to new synapses being formed
which causes integration of impulses
• Filter out less frequent impulses or low level stimuli
The neuromuscular junction
Muscle contraction at a neuromuscular junction
• Striated muscle contracts when it receives an impulse from a motor
neurone via the neuromuscular junction
• When an impulse arrives at the presynaptic membrane, the action
potential causes calcium ions channels to open in the presynaptic
membrane
• Ca2+ enter the presynaptic knob/motor end plate
• This stimulates vesicles containing the neurotransmitter acetylcholine
(ACh) to fuse with the presynaptic membrane
• Acetylcholine is released by exocytosis and diffuses across the cleft in the
neuromuscular junction
• Acetylcholine binds to receptors on the sarcolemma
• This stimulates Na+ channels in the sarcolemma to open and Na+ enter the
sarcoplasm
Muscle contraction at a neuromuscular junction (cont)
• This depolarises the sarcolemma, generating an action potential that
passes down the T -tubules towards the centre of the muscle fibre
• These action potentials cause voltage-gated calcium ion channel proteins in
the membranes of the sarcoplasmic reticulum to open
• Calcium ions diffuse out of the sarcoplasmic reticulum into the sarcoplasm
surrounding the myofibrils
• Calcium ions bind to troponin molecules, stimulating them to change shape
• This causes the troponin and tropomyosin proteins to change position on
the thin (actin) filaments
• The myosin-binding sites are exposed on the actin molecules
• The process of muscle contraction (known as the sliding filament can now
begin
The sequence of events that follows the arrival of an impulse at a
motor end plate
Role of mitochondria in the end plate of a
neuromuscular junction
• Synthesise ATP
• ATP is needed to synthesise acetylcholine
• ATP is needed for exocytosis of acetylcholine
• ATP is needed to transport calcium ions out of presynaptic neurone
into sarcoplasmic reticulum
• ATP is needed to synthesise acetylcholinesterase
• ATP is needed for Na+ pumps / active transport of Na+
Ultrastructure of striated muscle
• Striated muscle is skeletal muscle that is made of many muscle fibres
• Fibres are multinucleate
• Cell surface membrane is sarcolemma
• Sarcoplasm has many mitochondria
• Sarcoplasmic reticulum membranes have protein pumps that transport calcium
ions into the lumen of the Sarcoplasmic reticulum
• The sarcolemma has many deep tube-like projections that fold in from its outer
surface. These are known as transverse system tubules or T-tubule system. These
run close to the sarcoplasmic reticulum
• The sarcoplasm contains many myofibrils. Myofibrils are bundles of actin and
myosin filaments, which slide past each other during muscle contraction
• Thick filaments are made of myosin and are attached to M line
• Thin filaments are made of actin and attached to Z line
Ultrastructure of striated muscle (cntd)
• Interdigitation of thick and thin filaments causes striated appearance
• A band –darker parts of the stripes correspond to thick myosin filaments
and darkest parts are areas where myosin and actin filaments overlap
• I band – lightest part contain only thin actin filaments
• H bands – contains myosin filaments only
• M line is the attachment for myosin filaments only
• A sarcomere is the distance between Z lines
• Myosin is a fibrous protein with a globular protein head
• Actin is a chain of globular protein molecules
• Tropomyosin / troponin is attached to actin ;
The structure of a myofibril
Electron micrograph of an individual sarcomere
Parts of a myofibril
Structural features of thick and thin filaments
in a sarcomere
Thick filaments
• Made of myosin which is a fibrous protein
• Contains globular heads / ATPase
• 15 nm diameter
• Attached to M lines
Thin filaments
• Made of actin which is a globular protein
• Contain tropomyosin / troponin a binding site for myosin (head)
• 7 nm diameter
• Attached to Z lines
The sliding filament model of muscular
contraction
• The myofibril is stimulated to contract by the arrival of an action potential
• Calcium ions are released from sarcoplasmic reticulum
• The calcium ions bind to troponin
• This causes troponin to change shape and moves tropomyosin exposing the binding site on actin
• The myosin head, binds to site and forms cross bridge . This detaches ADP and the Pi from the
head
• The myosin head tilts and pulls actin /forms a power stroke.
• A new ATP molecule attaches to the myosin head causing the head to detach from actin
• This causes the myosin head to let go of actin
• The myosin head goes back to previous recharged orientation / re-cocks
• ATP hydrolysis causes the head to stand up/pivot
• The process is repeated
• The sarcomere shortens
Sliding filament model
of muscle contraction
Muscle contraction of single sarcomere
The role of the sarcoplasmic reticulum in the
contraction of striated muscle
• Ca2+ channels open
• Ca2+ diffuses into the sarcoplasm
• Ca2+ binds to troponin
• This causes tropomyosin to moves
• Cross-bridges form / myosin binds to actin
Role of calcium ions in shortening of
sarcomere
• When sarcoplasmic reticulum is depolarised calcium ion channels
open
• calcium ions released from sarcoplasmic reticulum
• Calcium ions move into sarcoplasm and bind to troponin
• Troponin changes shape
• Tropomyosin moves exposing binding site on actin
• Myosin head binds to actin
• Myosin head tilts / power stroke occurs
• Actin is pulled
How tropomyosin and myosin are each involved in
the sliding filament model of muscle contraction
Tropomyosin
• Tropomyosin uncovers, myosin binding sites on actin when calcium ions bind to troponin
• Tropomyosin moves allowing myosin to bind to actin / form cross-bridges
Myosin
• ATP hydrolysis / ATP → ADP + Pi causes the myosin head to, pivot / rotate / tilt / stand up
• The myosin / head, binds to actin / forms cross-bridges with actin
• ADP and Pi detach
• The myosin head, swings back / returns to previous position
• Actin is moved / power stroke occurs
• A new ATP binds to myosin head
• The myosin / head, detaches from actin / cross-bridges break
The role of ATP in the contraction of striated
muscle.
• Myosin head, binds to actin / forms cross bridge
• ADP released causes motion of myosin head which moves actin
• A power stroke occurs
• ATP binds to myosin head causing the myosin head to detach from
actin
• A cross bridge is broken
• ATPase causes, hydrolysis of ATP / ATP → ADP + Pi
• The myosin head tilts back to original position
• ATP is needed to pump Ca2+ back into sarcoplasmic reticulum ;
The Venus fly trap
• The Venus fly trap is a carnivorous plant that gets its supply of nitrogen and
phosphorous compounds by trapping and digesting insects
• The specialised leaf is divided into two lobes either side of a midrib -The inside of
the lobes is red and has nectar-secreting glands on the edges to attract insects
• Each lobe has three stiff sensory hairs that respond to being touched
Features of Venus flytrap
• Midrib = hinge
• 2 lobes
• glands that secrete digestive enzymes
• sensory hairs on each lobe that respond when they are deflected
• nectar-secreting glands to attract insects
• stiff outer-edges that interlock to trap insects
The Venus Fly trap
The Venus fly Trap- how insect is trapped
• The internal surfaces of leaf have sensory hair cells which are deflected when an insect
touches them
• Mechanical energy is converted to electrical energy
• The cell membrane depolarises if at least two hairs touched within 35 seconds
• This generates an action potential. The action potential spreads over the leaf lobe
• The action potential reaches to hinge / midrib cells
• This causes H+ to be pumped out of cells into cell walls . The cell wall loosens as crosslinks broken
• Calcium pectate dissolves (in middle lamella)
• Ca2+ enter the cells . This lowers the water potential of cells
• Water enters the leaf cells by osmosis
• The hinge cells expand / become turgid
• The leaf change from convex to concave shape and the trap shuts in quickly
Role of auxin in elongation growth
• Acid-growth hypothesis
• Auxin binds to a receptor molecule on the cell surface membrane
• Auxin stimulates proton pumps in the cell surface membrane
• H+ are pumped into cell wall by active transport which uses energy
• This causes the pH of the cell wall to decrease . The cell wall becomes more)acidic
• The pH-dependent enzymes activated
• This activates proteins known as expansins, which breaks the bonds between cellulose
microfibrils in the cell wall
• The cell wall loosens/becomes more elastic
• At the same time, K+ channels are stimulated to open
• This leads to an increase in K+ concentration in the cytoplasm, which decreases the water
potential of the cytoplasm
• More water enters the cell by osmosis
• This increases the turgor pressure of the cell
• The cell wall expands and the cell elongates
Auxins
• Plant hormones (also known as plant growth regulators) are
responsible for most communication within plants
• Auxins are a type of plant growth regulator that influence elongation
growth which determines the overall length of roots and shoots
• Auxin is synthesised in the growing tips of roots and shoots (i.e.. in
the meristems, where cells are dividing)
• Growth in these meristems occurs in three stages: cell division by
mitosis, cell elongation by absorption of water and cell differentiation
• Auxin is involved in controlling growth by elongation
Role of auxin in
cell elongation
Structure of the barley seed
The barley seed contains:
• An embryo -Produces gibberellins.
• An endosperm which is a starch-containing energy store surrounding
the embryo
• An aleurone layer which is a protein-rich layer on the outer edge of
the endosperm
Structure of the barley seed
Role of gibberellin in the germination of barley
• The seed is, dormant / metabolically inactive before onset of germination
When the conditions for germination are suitable :
• The seed absorbs water to begin the process of germination
• This causes the embryo to produce gibberellins
• Gibberellins diffuse into the aleurone layer
• Gibberellin stimulates the aleurone layer to produce amylase
• Gibberellin does this by regulating genes involved in the synthesis of amylase, causing an
increase in the transcription of mRNA coding for amylase
• Amylase hydrolyses starch in the endosperm to, maltose
• The maltose is converted to glucose and transported to the embryo
• The embryo uses the glucose for respiration
• The energy / ATP produced is , used for growth ;
How the secretion of gibberellins by the embryo results in the
mobilisation of starch reserves during germination
Role of amylase in seed germination
• Amylase hydrolyses / breaks down / digests / converts,
starch / amylose in endosperm to, maltose / glucose
• The glucose is used by embryo for, respiration / growth ;