Topic 8 Wood Flashcards
Nerve
bundle of the axons of many neurones surrounded by a protective covering
Neurone
nerve cell
Axons
long single structure taking impulses AWAY from the cell body
Dendrites
very fine and conduct impulses TO the cell body
Neurone basic structure
- cell body (nucleus. organelles etc)
- extensions: dendrites and axons
Nervous response (transmission, speed, type of change, method of action, type of response)
- transmission is electrical along neurone and chemical at synapse
- rapid acting
- usually a short term change (e.g. muscle contraction)
- usually a very local response, such as a specific muscle or gland
- method of action is by action potentials carried by neurones to specific cells
Hormonal (endocrine) response (transmission, speed, type of change, method of action, type of response)
- transmission by a chemical carried in the blood
- slow acting
- can control long term changes (e.g. growth)
- blood carries hormones to all cells but only target cell responds
- widespread response, such as growth and development
How can you tell the difference between types of neurones? Which is which?
depending on where their cell body is located:
Sensory - in centre, off to the side
Relay - in centre, in axon/ middle
Motor - in the end by dendrites
closer to dendrites, further along reflex arc
Cell that produces myelin sheath
schwann cell
gaps between schwann cells
nodes of Ranvier
What are the antagonistic pair of muscles in the eye called? What do they control?
radial muscles and circular muscles, they can increase/ decrease the size of the pupil
In dim light what happens to the pupil?
the pupil gets bigger, diameter increases, radial muscles contract
In bright light what happens to the pupil?
the pupil gets smaller, diameter decreases, circular muscles contract
The resting state of an axon is also called…
…the resting potential
What is the potential difference across a membrane when at resting potential?
-70mV –> the membrane is said to be polarised
Potential difference
All cells have a difference in electrical charge across the plasma membrane, this is the potential difference
When does a nerve impulse or action potential occur?
when the p.d across an axon is temporarily reversed, the p.d changes to around +40mV, the membrane is said to be depolarised
What voltage dependent channels are open/closed during different stages of action potential generation?
Potassium: resting potential - closed
depolarisation - closed
repolarisation - open
Sodium: resting potential - closed
depolarisation - open
repolarisation - closed
Positive feedback
is the sequence of events where a change in a system sets in motion processes which causes the system to change even further e.g sodium ions flowing into the axon triggers more gates to open and more sodium ions to enter
All or nothing - action potential
When an action potential is produced in a nerve cell, it is always the same size. It does not matter how big the initial stimulus the action potential will always involve the same change in p.d across the cell surface membrane
Refractory period
The short period of time after an impulse has passed along a neurone when a new action potential cannot be generated. It lasts until all the sodium ion and potassium ion channels have closed and the resting potential has been restored
Absolute refractory period
can’t generate any action potential
What is needed to generate an action potential?
enough of a stimulus - the threshold potential must be reached to generate an action potential
What happens if a strong stimulus is felt?
it results in more frequent action potentials - potential never exceeds +40mV
Resting potential step 1
-Protein carrier using active transport (sodium potassium pumps), 3 sodium ions pumped out of axon whilst 2 potassium move in
Resting potential step 2
-More positive ions are pumped out than in so a slight positive charge outside and more potassium ions inside
Resting potential step 3
-Membrane is more permeable to potassium so more K+ channels open than Na+ channels
Resting potential step 4
-More potassium ions inside so K+ diffuses out of the axon down the concentration gradient. As K+ move out they transfer positive charge
Resting potential step 5
-Overall negative charge inside due to presence of organic anions
Resting potential step 6
-Negative state inside the axon produces an electrochemical gradient causing K+ to be attracted to the inside
Resting potential step 7
-When no further net movement of K+ the potential difference across the axon is -70mV. The axon is polarised. This state is maintained until an impulse is present
Action potential step 1
-Depolarisation: When the axon is stimulated the voltage gated sodium channels open. Sodium ions flood in and disperse opening the next one. This means more come in and the cycle repeats (positive feedback)
Action potential step 2
Repolarisation: The sodium channels shut and the voltage dependent potassium channels open causing potassium ions to flood out of the axon. These remain open so the inside of the axon becomes too negative
Action potential step 3
Hyperpolarisation: The membrane is hyperpolarised (too far). Voltage dependent potassium channels close. Potassium diffuses back into axon to restore resting potential
Glandular system is also known as…
…endocrine system
Where do action potentials happen?
at the nodes of Ranvier - this is the only place ions can move so the impulse ‘jumps’ from one node to the next (this is much faster than a wave of depolarisation along the whole membrane)
Saltatory conduction
When the impulse appears to ‘jump’ from one node to the next because this is the only place the ions can move and the membrane be depolarised - this is much quicker than a whole wave of depolarisation
Explain consecutive action potentials (explains unidirectional) step 1
-Resting potential outside axon positive, high Na+, inside axon, negative, high K+
What causes the action potential to be unidirectional?
due to the refractory period so the impulse can only spread and depolarise in one way
Explain consecutive action potentials (explains unidirectional) step 2
-When stimulated Na+ voltage gated open, sodium ions flood in and spread out (membrane depolarises)
Explain consecutive action potentials (explains unidirectional) step 3
-Localised electric currents are generated in the membrane, change in charge in that part of the membrane
Explain consecutive action potentials (explains unidirectional) step 4
-Because of sodium flooding in causing a change in pd the second action potential is initiated from the first
Explain consecutive action potentials (explains unidirectional) step 5
-At the site of the first Na+ channels close, K+ channels open so K+ leave axon, repolarising membrane causing hyperpolarisation
Explain consecutive action potentials (explains unidirectional) step 6
-3rd action potential initiated by second. In this way local electric currents cause the nerve impulse to move along axon. At the site of the first action potential K+ diffuse back in restoring resting potential. At 2nd hyperpolarisation occurs, this is the refractory period so the impulse is unidirectional
What is the speed of the nerve impulse affected by?
- Axon diameter
- temperature
How does temperature affect the speed of the nerve impulse?
the higher the temperature, the faster the speed of the impulse - temperature affects the rate of diffusion of ions across the axon
How does axon diameter affect the speed of the nerve impulse?
The greater the diameter of the axon the faster the impulse travels. –> Axons with small diameters have a larger surface area to volume ratio compared to axons with wider axons. This causes a larger amount of ions to leak out the axon making it difficult for an action potential to propagate
Synapse
where 2 neurones meet
Synaptic cleft
separates a presynaptic and postsynaptic membrane
The nerve impulse can’t cross the gap between neurones, how does it travel across it?
by chemicals called neurotransmitters which carry the impulse across
What channels are on the presynaptic membrane?
calcium gated channels
What channels are on the postsynaptic membrane?
sodium gated channels
Nerve impulse across a synapse overview
- Action potential arrives
- Presynaptic membrane depolarises
- Calcium ion channels open
- Calcium ions flood in (enter neurone)
- High concentration of calcium ions cause synaptic vesicles containing neurotransmitter to fuse with presynaptic membrane
- Neurotransmitter is released into synaptic cleft (Acetylcholine)
- Neurotransmitter diffuses across gap and binds to receptors on postsynaptic membrane
- Sodium ion channels open and sodium ions flood in
- The postsynaptic membrane depolarises and starts an action potential
- The neurotransmitter is removed from the synaptic cleft
Main neurotransmitter (first to be discovered)
acetylcholine
Excitatory synapse
makes it more likely for an action potential e.g. make the postsynaptic membrane more permeable to sodium ions, lowers the threshold potential
Inhibitory synapse
makes it less likely for an action potential to occur - postsynaptic membrane less likely to depolarise e.g. closes sodium ion channels
What determines whether the next impulse is generated?
the net effect of all the impulses received by the postsynaptic cell - depends on:type of synapse, number of impulses received
What ultimately determines whether an action potential occurs?
the balance of excitatory and inhibitory synapses
Summation
each impulse adds to the effect of others
Spatial summation
The impulses are from different synapses (usually different neurones). The number of different sensory cells stimulated can be reflected in the control of the response
Temporal summation
Several impulses arrive having travelled along the same neurone. The combined release of neurotransmitter generates an action potential
What does the myelin sheath do?
insulates the axon preventing ion flow across the membrane
Nerve impulse across a synapse step 1
An action potential arrives at the presynaptic neurone
Nerve impulse across a synapse step 2
The presynaptic neurone depolarises causing calcium channels to open and calcium ions to flood in to the axon (at the terminal end)
Nerve impulse across a synapse step 3
The increased level of calcium in the cell causes the synaptic vesicles to move towards the pre-synaptic membrane
Nerve impulse across a synapse step 4
The vesicles contain the neurotransmitter, so when the vesicles fuse with the membrane the neurotransmitter enters the synaptic cleft by exocytosis
Nerve impulse across a synapse step 5
The neurotransmitter diffuses across the synaptic cleft binding to receptors on sodium ion channels on the postsynaptic membrane. These channels open and sodium ions flood in to the postsynaptic neurone
Nerve impulse across a synapse step 6
The postsynaptic membrane depolarises. If a threshold value is reached an action potential is generated in the postsynaptic neurone.
Nerve impulse across a synapse step 7
Acetylcholine is broken down into ethanoic acid and choline by the enzyme acetylcholinesterase (found in the synaptic cleft). Choline and ethanoic acid diffuse back into the presynaptic neurone. ATP from mitochondrion is used to recombine them to acetylcholine, the synapse can now transmit another action potential
Blind spot
no cone cells here –> no photosensitive cells, all axons join together at this point by the optic nerve
Fovea
most sensitive part of the retina located within the macula, the central area of the retina - mainly cone cells
What are the two types of photoreceptors in the human retina?
rod cells - black and white vision in dim and bright light
cone cells - colour vision in bright light
What are the 3 layers making up the retina?
- rods and cones synapse with bipolar neurones
- bipolar neurones synapse with ganglion neurones (axons of ganglion neurones make up optic nerve)
- light hitting retina has to pass through layers of neurones before reaching rods and cones
Rod cells key features
- work well in low light conditions
- monochrome vision
- light sensitive chemical is rhodopsin (contained in membrane bound vesicles)
- are found throughout the retina but not on the fovea or blind spot
Cone cells key features
- only work in bright light
- colour vision
- light sensitive chemical is iodopsin (contained in membrane bound vesicles)
- 3 types of cone cells which are all sensitive to different wavelengths of light: red, green, blue
How do the 3 types of cone cells allow us to see different colours?
they contain different forms of iodopsin in each type of cone cell that are sensitive to different wavelengths of light so the colour seen depends on relative degree of stimulation of different types of cone cell
Rod cells in the dark
- Na+ flow into the rod through open cation channels
- Na+ move along the cell (down the concentration gradient)
- Na+ is actively pumped out of the cell
- The membrane becomes slightly depolarised from -70mV to -40mV
- This causes continuous release of the neurotransmitter (glutamate)
- The neurotransmitter binds to the next cell (bipolar cell) and prevents it from depolarising preventing an impulse (inhibitory synapse)
Rod cells in the light
- rhodopsin + light –> retinal + opsin
- opsin causes Na+ channels to close
- Na+ can’t get in
- Na+ still actively pumped out
- Inside the membrane becomes more negative (hyperpolarised)
- Stops the release of glutamate
- Cation channels in the bipolar cell open, sodium ions flood in and the cell depolarises
- Action potential (nerve impulse) starts (in a neurone which is part of the optic nerve)
Glutamate
the principle neurotransmitter in the brain
What needs to happen after rhodopsin is broken down?
After being broken down in the light, rhodopsin needs to be converted back to its original form. This takes a few minutes, the higher the light intensity the longer it can take rhodopsin to reform (brightly lit to dimly lit, unable to see anything while rhodopsin reforms)
Phytochromes
- chemical that changes in response to light
- consists of protein component bonded to non-protein light absorbing pigment
Phytochrome red
absorbs red light; 660nm
Phytochrome far red
absorbs far red light; 730nm
In what form is the phytochrome synthesised in plants?
its synthesised as phytochrome red
What happens when you shine different lights on phytochrome red?
shine red light on Pr, it turns to Pfr
shine far red light on Pfr, it turns to Pr
dark on Pfr, trickles back to Pr
Process in which phytochromes act as transcription factors
- exposure to light causes change in form of phytochrome
- phytochrome changes shape
- this allows interaction with other signal proteins
- the signal proteins act as/ activate transcription factors
- these can bind to DNA to regulate light sensitive genes
- this controls the production of light sensitive proteins
What is a key trigger for flowering time in many plants?
number of hours of interrupted darkness
Long day plants
- flower in summer
- uninterrupted darkness for less than 12 hours
- flowering needs Pfr
Short day plants
- flower in spring or autumn
- uninterrupted darkness for more than 12 hours
- flowering inhibited by Pfr
- long hours of darkness convert Pfr to Pr
- a short burst of red light negates the dark period
What does the ratio of Pfr to Pr enable a plant to do?
to determine the length of day and night and when to flower
Nervous system in animals - response
- electrochemical changes –> electrical impulse
- rapid
- very local and specific
Endocrine system in animals - response
- chemical hormones from glands carried in blood plasma
- slower
- can be widespread or restricted to target cells
Tropisms in plants - response
- chemical growth substances diffuse from cell to cells/ phloem
- slower
- may be widespread but usually restricted to cells within a short distance of substance release
Exocrine glands
secretes substance onto a surface usually through a duct
Endocrine glands
secretes substance into the bloodstream (no ducts)
Glands of the endocrine system
Pituitary gland - LH, FSH Thyroid gland - thyroxin Pancreas - glucagon, insulin, digestive Adrenal glands - adrenaline Ovaries - oestrogen, progesterone Testes - testosterone
Mammalian hormones
- are released directly into the blood plasma from endocrine glands
- have specific target cells
- slow, long-lasting, widespread response
How do hormones work once they reach the target organ?
it affects the target cells by attaching onto specific receptors either on the surface of or within the cells
Exocrine glands features
- present throughout the body
- contain ducts
- carry products straight to target cells on epithelial layers of internal/ external body surfaces
- don’t produce hormones; secrete other products e.g. sebum onto skin, gastric juice onto stomach lining
Overall brain structure
- outer layer is the cortex
- it consists of grey matter
- it is highly folded and divided into left and right cerebral hemispheres
- each hemisphere has a number of regions called lobes
- the two hemispheres are connected by a band of white matter called the corpus callosum
The brain stem is also called…
…the reptilian brain
What does the brain stem control?
essential functions for survival e.g. heartbeat, breathing, digestion, body temperature, sleeping and walking
Cerebellum function
responsible for balance, co-ordinates movement
Midbrain function
relays info to the cerebral hemispheres e.g. auditor to temporal lobe, visual to occipital lobe
Medulla oblongata function
regulates and controls heart rate/ heart beat and blood pressure; detects changes in pH due to CO2 levels in blood and uses this to regulate breathing
Hypothalamus function
thermoregulation (both core and body temp), hunger, sleep, thirst (is also part of the endocrine system secreting hormones with a direct link to pituitary gland)
Cerebral hemispheres function
ability to see, think, learn and feel emotions
What are the 4 lobes in each cerebral hemisphere?
Frontal lobe, temporal lobe, occipital lobe, parietal lobe
Thalamus function
responsible for routing all the incoming sensory information to the correct part of the brain
Hippocampus function
laying down long term memory
Basal ganglia
are a collection of neurones that lie deep within each hemisphere and are responsible for selecting and initiating stored programmes for movement
Parietal lobe function
concerned with orientation, movement, sensation, calculation, some types of recognition and memory
Occipital lobe function
concerned with processing information from the eyes including vision, colour, shape, recognition and perspective
Temporal lobe function
Concerned with processing auditory information e.g. hearing, sound, recognition and speech. Also involved in some memory
Frontal lobe (including the prefrontal cortex)
Concerned with higher brain functions such as decision making, planning, reasoning and emotions. Is also involved in making associations and creating ideas. Has neurones connecting directly to brain stem and spinal cord so controls movements and stores info on learnt movements
Why does the pupil appear black?
because pigment at the back of the eye absorbs light
Reflex arc
stimulus, receptors, sensory, relay, motor neurones, effector
Critical windows/ periods
- are periods when the nervous system needs specific stimuli to develop properly
- are periods of time during which vital neural connections are made in response to specific stimuli
- if the brain doesn’t receive these stimuli at the crucial time the pathways will not develop normally
Light –> Eye –> Brain
-light enters the eye
-light is converted to an electrical signal
-signal passes out of the eye through the optic nerve
-will travel to the thalamus, then:
some goes to the visual cortex fro processing
some goes to the Midbrain for link with motor neurones involved with pupil dilation and eye movement
some links with auditory nerves to allow eyes to move in direction of sound
What does the brain need after birth?
much development through the growth of axons and formation of synapses
What is postnatal brain growth due to?
- axon elongation
- myelination
- synapse development
What needs to happen for vision to develop (after day 21 when your brain is fully formed)?
neurones need to make the correct connections
Where does evidence for the critical period come from?
- medical observations
- animal models
What happens if a baby has a bandaged eye?
will have permanently damaged vision
Why is it that if elderly people develop cataracts, if removed they have no effect on their vision but if in a young child the eye will be permanently impaired?
elderly people are post the critical period so will have normal vision when the cataract is removed but in a young child if not removed before 10 years old the eye will be permanently impaired and unable to perceive shape or form
Animal models
- animals which have been studied extensively so that we know a lot about them
- used because of the ease of breeding, small size and short lifecycle (fruit flys, zebrafish)
- others are used due to similarity to humans (mice, rats, cats, monkeys)
- this can raise ethical issues
Newborn animals (model)
- Monkeys were raised in the dark, light with no patterns and normal light. Former 2 had problems with pattern recognition
- Monocular deprivation (deprive light stimulus in one eye) of newborn monkeys. Hubel and Wiesel found that monkeys were blind in one eye. The retinal cells responded normally to light but the visual cortex didn’t respond
- Found then that all that was needed was deprivation for a critical period of 1 week to have the same effect
- Deprivation in adult monkeys had no effect
Kitten testing
under 3 weeks - no effect (normal eyesight)
after 3 months - no effect
at four weeks - major effect even if only for a few hours
we can deduce that a kitten’s critical period is between 4 weeks and 3 months
During the critical period…
-the columns in the visual cortex are the same width for normal conditions, dendrites and synapses from light stimulated eye take up more territory in the visual cortex so light stimulus required for full development of visual cortex
During the critical period continued… (if an eye is deprived of light then…)
- If an eye is deprived of light then the columns corresponding to that eye are narrower
- Axons compete for target cells to create synapses within the visual cortex
- In non stimulated eye the associated axons are not stimulated and don’t form synapses; these axons are eventually lost
- There are more neurones than needed; in retina up to 80% die during developement
How is territory of non stimulated eye reduced
Every time a neurone fires onto a target cell, the synapses of another neurone sharing the target cell are weakened and they release less neurotransmitter. If this happens repeatedly the synapses not firing will be cut back
Learning
- a relatively permanent change in behaviour or knowledge that comes from experience
- underpinned by changes occurring in the network of neurones especially at the synapses
Memories are stored…
- not localised - in many parts of the brain
- different places for long and short term memory
- can be studied through medical examples –> treatment of epilepsy, removed parts of the brain, led to amnesia, long term memories unaffected, no new ones made
What are the 2 ways memories can be created?
By altering: the pattern of connections, the strength of synapses (more connections, repeated use of synapses, creating of additional synapses)
Making memories is an active process
What did Eric Kandel do?
- investigated giant sea slugs
- they share similar nerve cells and synapses to humans but less neurones
- they have no saltatory conduction - so small myelination not very advantageous
- looked at gill reflexes
Aplysia habituation
- Gill is withdrawn in a jet of water as a protective reflex
- Habituation happens if repeatedly stimulated by a jet of water –> they withdraw gills less and eventually hardly at all
- Found that the amount of neurotransmitter changed
What is habituation?
a type of learning
ignore unimportant repetitive stimuli so limited sensory response, attention and memory resources can be concentrated on more important things
Full development of the eye –> brain information
- There is a lack of visual stimulation in one eye
- Axons from the visually deprived eye do not pass impulses to cells in the visual cortex so no neurotransmitter released
- Axons from the non deprived eye pass impulses to cells in the visual cortex so neurotransmitter released
- Synapses made by active axons are strengthened so release more neurotransmitter
- Inactive synapses are eliminated
- So for full development of the visual cortex nerve impulses from both eyes and neurotransmitter release from all neurones involved must occur
Blood Brain Barrier
semi-permeable membrane separating blood from the cerebrospinal (extracellular brain) fluid - a barrier to the passage of cells, particles, large molecules
How does the bbb prevent entry?
network of blood vessels that allows entry of essential nutrients while blocking other substances
What does the bbb block and allow? How?
Allows - glucose, hormones, oxygen, carbon dioxide, soluble molecules
Blocks - toxins, bacteria, often life saving drugs
Endothelial cells restrict diffusion of microscopic objects which are large and hydrophilic
Why is the bbb an issue?
because it often blocks life saving drugs from reaching the brain, antibodies and antibiotics are too large to cross as well so infections of the brain are very serious and difficult to treat
Neurotransmitter examples
amino acids, dopamine, noradrenaline, adrenaline, histamine, serotonin, acetylcholine
Depression and Parkinson’s disease
- both are caused by chemical imbalances in the brain: depression - serotonin, Parkinson’s - dopamine
- both can have a genetic link: Parkinson’s due to mutations in one of several identified genes
- both are multifactorial; genes and environment
Ecstasy stage 1
-Serotonin transporters are responsible for removing serotonin molecules from the synaptic cleft (into presynaptic membrane)
Ecstasy stage 2
-Ecstasy mimics serotonin and is taken up by serotonin transporters. In fact ecstasy is more readily taken up than serotonin itself
Ecstasy stage 3
-The interaction with ecstasy alters the transporter; the transporter becomes temporarily reversed. The transporter starts transporting serotonin out of the cell
Ecstasy stage 4
-The excess of serotonin becomes trapped in the synaptic cleft. As a result it binds again and again to the receptors (on post synaptic membrane) - overstimulating the cell
Ecstasy stage 5
-Ecstasy affects serotonin pathways responsible for mood, sleep, perception and appetite. Also indirectly interacts with reward pathway –> milder dopamine release makes ecstasy slightly addicitive
Parkinson’s disease Stem cell therapy
- cure rather than palliative treatment
- embryonic stem cells could replace failing dopamine producing cells
- research has been conducted using mice and has been promising
- ethical issues remain
- safety issues; uncontrolled growth
Parkinson’s disease gene therapy
- human genome project
- possibility of inserting healthy genes into affected cells
- add genes to prevent dopamine producing cells from dying or add genes to boost dopamine production in remaining cells
- biggest problem is delivering genes to target areas of the brain
- side effects unknown
Absolutist view
a belief that animals should never be uses
Utilitarianism (rationalist view)
the belief that the right course of action is the one that maximises the amount of happiness/ pleasure in the world - certain animals could be used for medical experiments provided that the expected benefits are greater than the expected harm
Conditions of rationalist experiment
certain amount of animals - no more certain way/ method reach suitable conclusion strict guidelines (only used if no other way)
Genetically modified organism
an organism that has been genetically engineered by the artificial introduction of genetic material from a different organism
An organism has had genetic material added to it from another organism what is the resulting organism called?
transgenic and is referred to as a GMO
Transgenic
modification of a gene within an organism
Why is genetic engineering better than artificial selection?
because artificial selection is a long process and the use of genetic engineering to introduce alleles can reduce the development times
Novel approaches to plant breeding:
- proteins for healing wounds
- chemicals to treat CF, cirrhosis of liver and anaemia
- plants that contain antibodies, rabies, foot and mouth, cholera
GM animals
- a range of methods can be used including inserting new DNA directly into the embryo
- Tracey was the first transgenic human/ other species animal
- Work being carried out will breed sheep so that milk can be produced which contains useful proteins
- Chicken as ‘biofactories’ to produce useful chemicals in their egg whites
- sometimes referred to as pharming
How are genes transferred in plants?
- minute pellets that are covered with DNA carrying the desired genes are shot into plant cells using particle gun
- scientists insert desired genes into a plasmid which then ‘carries’ these genes into the plant DNA
- viruses are sometimes used, they infect cells by inserting their DNA or RNA. They can be used to transfer the new genes into the cell
Protoplast
plant cells with cell walls removed by enzymes
Human genome project
deciphering the base sequence of the human genome - much better understanding of the way genes control our phenotype, so major advances in understanding and treating of diseases
Genome
all the DNA of an organism
Drug target
specific molecule that a drug interacts with to bring about its effect
Personalised medicine
- normally prescribing a drug is trial and error at best; in some people its effective, in others not or some people experience side effects and others don’t
- this is because of variations in everyone’s genome
- information about a person’s genome allows doctors to prescribe the right drug at the correct dose
- if a person knew they carried mutations for a disease they could change their lifestyle to reduce the risk
- revolutionise diagnosis, treatment, prevention of disease
Plasmids GM
plasmid removed from bacterial cell, using restriction enzymes plasmid is cut, then using other enzymes a piece of DNA from another organism can be inserted into it, the plasmid is reinserted into bacteria which multiply and protein produced is extracted from culture
Pellets GM
- plasmid is removed from bacterial cell
- plasmid is cut with restriction enzyme
- gene of interest is cut from DNA with restriction enzyme
- gene inserted into plasmid along with antibiotic marker
- coat particles with the plasmid and coat bullet with particles
- gene gun is fired at plants where the foreign gene will be incorporated into plant chromosome
- plate cells on a growth medium with antibiotic; only transformed cells will be selected
- micropropagation
- plantlets grow into plant
Bacteria GM
- plasmid is removed from bacterial cell
- plasmid is cut with restriction enzyme
- gene of interest is cut from DNA with restriction enzyme
- gene inserted into plasmid along with antibiotic marker
- plasmid is reinserted into bacteria
- allow bacteria to introduce plasmid into plant cell
- foreign gene incorporated into plant chromosome
- plate cells on a growth medium with antibiotic; only transformed cells will be selected
- micropropagation
- plantlets grow into plant
Why is a marker gene incorporated?
to screen if the foreign gene has been taken up and kills any which haven’t in GM plants
