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Description
Flashcards by Kristi Brogden, updated more than 1 year ago
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Created by Kristi Brogden
over 10 years ago
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| Question | Answer |
| What was sperry's hypothesis? | Chemoaffinity hypothesis 'Directed and specific outgrowth occurs through axons following 'individual identification tags' created by the cells and fibres of the embryo' |
| What was weiss's hypothesis? | Resonance theory 'Stochastic and diffuse neuronal outgrowth occurs to all targets followed by elimination of non-functional connections' |
| What proof is there that sperry was right? (3) | 1) Sperrys frog experiment 2) Axon pathways in embryos are highly stereotyped 3) Motor axons are guided specifically to their targets in the chick embryo |
| Describe sperry's frog experiment and its results | Cut optic nerve and remove temporal retina (allows just nasal axons to grow back) Importantly, the regrowing ‘red’ axons grew through, yet ignored the territory normally innervated by the ‘blue’ axons. The axons grew back directly to the right place |
| Describe an experimental approach that shows us that motor axons are guided specifically to their targets in the chick embryo | |
| What are the main ideas involved in the labelled pathway hypothesis? | 1) Axons can selectively fasiculate with other axons 2) Axon surfaces carry labels or cues 3) Different axon growth cones express different sets of receptors for such cues 4) Early axons (pioneers) form an axon scaffold on which later axons (followers) can extend |
| Describe an example of the importance of axon scaffolds in vertebrates | |
| Describe evidence from the grasshopper embryo limb that pioneer axons also follow stereotyped paths | The pioneer Ti1 (tibial1) growth cone makes a specific turn at the limb boundary, and then again as it approaches a specific cell, Cx1. Ablation of Cx1 causes the Ti1 growth cone to stall at the other side of the limb boundary. Neither Cx1 nor the limb boundary cells are distinguished by any obvious morphological features - there must be molecular differences in the enviroment. |
| What boundries do axons follow in the forebrain? | Boundries of domains of patterning gene expression. |
| What boundries do axons follow in the hindbrain? | Follow boundries of rhombomeres |
| What boundries do axons follow in the spinal cord? | Axons are attracted to, and follow boundries of the floor plate. |
| What are the four forces of axon guidance? | |
| How are the actin bundles arranged in lamella(podium)? | The actin bundles are crosslinked into a net |
| How are the actin bundles arranged in filopodia? | The actin bundles are polarised to form larger bundles. |
| Describe a model of how actin treadmilling may control filopodial extension? | |
| What happens to F-actin when a growth cone collapses? | It destabilises |
| What are 2 of the main different 'flavours' of semaphorins? | Can be: 1) Membrane-bound (As on retinal axons) 2) Secreted (e.g. Sema3A) |
| Which type of semaphorins can cause growth cones to turn? | Sectreted/soluble semaphorins |
| What is laminin and where is an example of where it is localised? | laminin is a growth-promoting extracellular matrix protein that is localised in the optic nerve |
| What is the evidence that laminin only dictates where axons can grow, not the direction of axon growth? | 1) Blockade of receptors for actin slows down the growth of retinal axons, but does not change their direction 2) Gradients of laminin in vitro do not direct axon growth - In fact we find that laminin is permissive for growth only within a specific concentration range. |
| What is the evidence that non-permissive factors such as semaphorins can channel axon growth? | |
| What are ephrins? | Non-permissive, contact repulsion factors used in early patterning and to guide axons. They are detected by receptors called ephs |
| What is netrin? | A secreted protein similar to laminin, which can associate with the extracellular matrix |
| What evidence is there that axons reprogram when intermediate targets (choice points) are encountered? | After transit of the midline, commissural axons lose responsiveness to netrins i.e. Sensitivity of axons to floor plate (netrins) changes after midline is crossed. |
| What evidence is there that axons reprogram when intermediate targets (choice points) are encountered? | Commissural axons also become sensitive to repellants after crossing floor plate |
| What does the roundabout gene robo encode and where is it expressed? | Robo, encodes a receptor for the inhibitory protein Slit. Robo protein is expressed at high levels on axons that don’t cross the midline. Commissural axons initially express low levels but high levels after they cross. |
| What happens in robo mutants (no robo protein made) | Slit is no longer detected, so all axons go back and forth across the midline forming Roundabouts of axons |
| Where is comm expressed? | Comm is expressed only in those neurons that normally cross the midline and is switched off after they cross. |
| What happens in a comm mutant (comm missing) | When Comm protein is missing (Comm mutant), Robo protein is expressed at high levels in those cells that would normally cross the midline, and which now extend their axons longitudinally |
| What happens if comms expression is forced in all neurons? | If Comm’s expression is forced in all neurons, Robo protein is lost everywhere resulting in a phenotype just like the Robo mutant. |
| How is robo prevented from functioning before midline crossing in flies and mice? | Comm encodes a “trafficking” protein that prevents Robo protein from reaching the cell surface |
| Why is robo prevented from functioning before midline crossing in flies and mice? | So that the growth cone cannot receive Slit inhibitory signals before crossing. |
| Where and when is the vertebrate homolog robo1 expressed? | It is expressed on comissural axons. However, it is expressed both before and after crossing. |
| What is the comm homolog in vertebrates? | There isn't one. However, a second Robo-like protein. Rig1 (aka Robo3), is expressed only in the pre-crossing fibres and appears to block Robo1 signalling until the midline is crossed. Loss of Rig1 results in a failure of C axons to reach the midline (floor plate) |
| What does Fasciclin II control? | It controls fasiculation in flies |
| How do we know that Fas II adhesion also controls defasciculation? | Overexpression of Fas II leads to a “By Pass” phenotype where the red and blue motor axons fail to defasciculate and so miss their targets (muscles 6, 7 and 13) |
| What are the two types of targets? | 1) Discrete targets (cellular) 2) Topographic maps (Multicellular) |
| What evidence is there for discrete targets? | |
| What are topographic maps? | When neighbouring neurons send axons to neighbouring sites in their target to maintain the topology (order) in the target, e.g. retinotectal system |
| What were sperrys theories about how topographic maps are acheived? | 1) Each axon has a unique label complementary to a unique label in the target. (cf address labels in fly muscle) 2) That a co-ordinate system, encoded by gradients of signalling molecules, stamps a "latitude and longitude" onto cells of the target which is read by complementary gradients of receptors expressed in the retinal ganglion cells. |
| Why is the labels theory implausible? | The number of labels required seems impossibly high |
| What evidence is there for gradients? | The “Stripe Assay” shows that cells from posterior tectum make a non-permissive factor that repels temporal retinal axons |
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