AVE stuff Flashcards
what should an organiser be able to do?
NAME?
what is the difference between a BL transplanted from an early gastrula as opposed to from a later gastrula?
NAME?
what do the cells from the blastopore lip go on to form in the xenopus?
anterior endoderm, prechordal late, head mesoderm, notochord
where is head inducing tissue found in the early blastula?
in the dorsal vegetal region- the presumptive anterior endoderm- acts as the AVE
what do the AVE cells express in the mouse?
crescent, cerberus, frzb, otx2, hex- they are involved in head patterning
where is cerberus expressed in xenopus?
anterior endoderm
how does cerberus block BMP WNT and Nodal?
binds to them outside the cell
how is neural induction different in the chick than in the xenopus?
BMP inhibition can not replicate the actions of the node to induce neural tissue- they can stabilise sox 3 expression after 5 hours but that is it- there is a different mechanism for neural induction- involving FGF from the node and from the underlying hypoblast
how has the organiser beens how to not be required for neural tissue in xenopus and what has been proposed as a result?
a neural plate will still develop in frogs, birds and mice the organiser or node is excised during gastrulation, although chordin and noggin encode for neural inducing signals in zebrafish, double knock out does not prevent a neural plate from developing - therefore it has been suggested that neural fate is given before gastrulation- maybe involving the WNT signalling in the early dorsal patterning of the xenopus embryo
what pieces of evidence suggests that gene expression in the mesoderm may be influencing gene expression in the in the ectoderm?
several box genes int he notochord and in the pre-somatic mesoderm and ectoderm are at the same position along the axis.
where can hox gene expression not be found in the mouse and what is thought to act in their place?
it can’t be found in the anterior most neural tissues such otx and em are expressed anterior to the hindbrain and these gene encode homeodomain TFs and specify th pattern of the neural plate
what is the simple two step process by which neural patterning is thought to occur along the neural tube?
mesoderm induces the antire overlying ectoderm to become anterior and then posteriorising signals transform the posterior parts of tissues after.
what are the posteriorising tissues thought to be?
FGf ants WNT3a
what are the two signals implicated in AP neural tube patterning ?
the first are the anterior signals thought to be noggin ad chordin, the second are the posteriorising such as FGF and WN3a
how do the node and the hypoblast act together to induce the AP axis along the neural tube in the chick?
the node emits FGF and posteriorisig signals, the anterior neural tissue must be protected from these signals- the anterior mesoendoderm is though tot achieve this as it moves anterior to the node after ingression and releases factors such as cerberus, frzb, dkk etc
what are the two organiser within the neural plate, what are their roles?
One of them is the anterior neural ridge, which lies at the junction between the prosencephalon and the anterior ectoderm, and is necessary for the maintenance of forebrain identity. The second one is the isthmic organizer (IsO), which lies at the junction between the midbrain and hindbrain, and is necessary and sufficient, for the development of mesencephalic and metencephalic structures.
what does the anterior neural ridge express?
FGF8, otx2, chordin, shh,
what is the Anterior neural ridge essential for? how has this been shown?
patterning of the telencephalon, removal of it in fish or mice will result in lack of forebrain expression of the telencephalon marker and gratifying an ectopic one into the diencephalon will induce telen marker expression
what is the role of the isthmus organiser? how was this shown?
found at the midbrain hindbrain junction, if you transplant it, it will induce the formation of an ectopic midbrain in the hindbrain
what is found in both the anterior neural ridge and the isthmic organiser?
FGF8
what is different about the neural induction in the chick and in the xenopus?
it doesn’t occur by default in the chick- BMP inhibition is not sufficient- instead it is a multiple step process
what is the FGf signalling pathway?
FGF TK receptor -grb, SOS, RAS, RAF, MAPKK, MAPK, acts with TF
what does the prechordal plate underly?
the anterior forebrain
what does the notochord underly?
the ventral head mesoderm
what is the neural default model?
this proposes that the defualt model of neural induction in xenopus. this proposed that the default stae of the dorsal ectoderm was to develop as a neural tissue but this pathway is blocked by the presence of BMPS which promote epidermal fate. The role of the organiser so to lift this block by producing proteins that inhibit BMP actvity, the region of ectoderm that comes under the influence of the antagonist form the organiser act on ectoderm and cause it to form neural tissue. according to this model the signals from the organiser act on the ectoerm that lies adjacent to the organiser at the bedginning of gastrulaion. as gastrulation process, internalises cells continue to act on the ectoderm that now overlies them.
what does the elimination of one BMP antagonist do compared to all 3?
when you remove 1 no effect but when you MO against them all- ventralise
explain how FGF has been implicated in neural induction the xenopus?
- neural development in xenopus also required FGF when even BMP is lifted by noggin or chordin. FGF is produce by cells in the blastula that are thought to act as early neural inducers. - it has also been shown that apparently spontaneous differentiaiton of explanted newt ectoderm into neural tissue is caused by activation to the MAPK pathway, this occurs in the FGF signalling pathway and treatment of explanted newt ectoderm with small molecule inhibitors of the pathway prvents neural differentiation. the ras-mapk pathway is also activated when xenopus extodermal cells are dissociated which might explain as noted ealrier hwy this dissociation forms neural fate so easily. induction of the neural plate therefore needs not only the antagonism of BMP signalling but also FGF siganlling (like in chick!)
how is FGF signalling though tot act in the neural patterning of the chick?
the effects of FGF neural induction may result from a direct inducting effect, activated MAPK can interefere with BMP signalling by causing an inhibitory phoshprylation of smad 1 which is part of the intracellualr BMP sgnalling pathway.
describe the ‘qualitative’ and ‘quantitative’ components of neural plate AP patterning
qualitative= the mesoderm secrets different antagonists at different points along the AP axis- it secretes BMP, Nodal and WNT inhibitors at the very anterior. But then only BMP antagonists are secreted more posteriorly, thought to induce spinal cord. quantitative: WNt/b-cat signalling along the AP axis is the neurula acts int a posterior to anterior graded manner, injected animal cap explants with different levels of NWT produces different posterior markers. FGF is also a posteriorising factor in a gradient.
in c.elegans, how can you take advantage of the transplicing?§
you can put an intercismronic region (SL2) in between your protein that yu are translationally reporting and you GFP gene
