Skip to content
Login Register

#cell fate determination

3 public questions tagged with this topic.

Morphogen Induction-l

Which experiment demonstrated that morphogen gradients determine cell fate?

Proof that graded morphogen concentration determines fate came from Xenopus animal cap experiments where defined doses of recombinant Activin elicited distinct mesodermal and endodermal programs. Low Activin induced ventral mesoderm and pan-mesodermal marker Xbra, intermediate induced muscle and MyoD, high induced organizer genes goosecoid, chordin and notochord plus endoderm markers Sox17. Dose-response mirrored embryonic distribution of endogenous Activins and Nodal-related signals from vegetal hemisphere, demonstrating quantitative threshold responses and differential enhancer affinity. Griffith, Hershey-Chase, Avery-MacLeod-McCarty experiments concerned DNA as heredity material. Activin titration remains classic vertebrate morphogen demonstration linking gradient to discrete fate specification.

Ref: Green and Smith, Nature 1990, Activin Concentration Determines Xenopus Cell Fate.

View Details
Elegans -ll

Which protein is essential for E cell fate in C. elegans?

E cell, posterior daughter of EMS, requires combinatorial inputs from SKN-1, MED-1/2 and Wnt-modified POP-1 to activate end-1 and end-3 GATA factors specifying intestine. Maternal SKN-1 activates med genes broadly in EMS lineage; Wnt signal from P2 causes reduction of POP-1 in E, converting it from repressor to coactivator with SYS-1 beta-catenin. Modified POP-1 together with SKN-1 induced MEDs binds endoderm enhancers, driving END-1/3 expression. POP-1 null causes both EMS daughters to become E-like, revealing essential role in distinguishing MS versus E. Hence POP-1 essential for activating E fate in cooperation with Wnt signaling pathway.

Ref: Maduro et al. 2005; Gilbert Chapter 4: POP-1 essential for E cell fate specification in C. elegans endoderm.

View Details
Elegans -ll

Which morphogen gradient influences primary and secondary vulval cell fates?

Primary and secondary vulval fates are graded by LIN-3/EGF morphogen secreted from anchor cell. LIN-3 forms diffusion gradient highest at P6.p overlying AC, intermediate at P5.p and P7.p, low at distant P3.p, P4.p, P8.p. High concentration surpasses threshold activating LET-23 EGFR to MAPK to LIN-1 inhibition, driving primary genes egl-17. Lower LIN-3 combined with lateral LIN-12 Notch activation specifies secondary fate expressing secondary markers. Experimental expression of LIN-3 under heat-shock promoter induces ectopic primary cells proportional to dose, demonstrating morphogen interpretation. Therefore LIN-3 gradient patterns 3-2-1-2-3 array in competent group.

Ref: Katz et al. 1995; WormBook: LIN-3 EGF morphogen gradient influencing VPC fates.

View Details