Ectoderm fate (neural or epidermal) Flashcards
Spemann and Mangold
- implanted donor cells from dorsal lip of blastopore into other side of host
- secondary neural tube develops where cells were implanted
- neuralization factor in dorsal lip
-epidermalization=default fate, implant induces neural
Need to ID neuralization factor
IDed noggin as neural inducer
-UV blast resulted in no nervous system
-treated with Li=hyperdorsalized embryo
-extracted polyA mRNA from hyperdorsalized and implanted in UV treated embryo
-isolated noggin cDNA->noggin protein+A->neural genes
Spemanns organizer
dorsal lip of the blastopore
neuralization via blocking dominant negative receptor (activin)
pre-gasturla=not determined
-mRNRA was injected for truncated activin receptor (not normal signaling)
->RESULTED IN NEURAL TISSUE
->if epidermal was default, then the tissue should have been epidermal
-dissociated animal cap prior to gastrulation
-secrete a factor that ins’t being received due to distance->results in neural cells
-intact animal cap, factor is recieved->epidermalization
Conclusion
-neural=default
-signaling pathway is related to activin signaling
->induces epidermal fate
-mesoderm secretes an unknown factor that inhibits an activin related signaling pathway
sog
neuralization
sog interacting with dpp
antagonize each other
dpp
epidermalization
BMP-4
homolog to dpp
-epidermalization
-overexpression=no neural cells
-addition of BMP4 to dissociated animal cap cells results in epidermal cells
Current mode of neural induction
-noggin binds to BMP4 and blocks it from binding to receptor
-results in neural cells
-BMP4 +receptor=epidermal cells
what supports current mode of neural induction?
- BMP4 administration to dissociated cells resulted in epidermalization
- BMP4 suppression experiment led to neural differentiation of animal caps without any inducers
BMP4 +activin
forms heterodimer
-truncated activin=non functional BMP4
->results in neural cells