TY  - GEN
T1  - ICD-1/BTF3 antagonizes SKN-1-mediated endoderm specification in Caenorhabditis elegans
AU  - Ewe, Chee Kiang
AU  - Torres Cleuren, Yamila N
AU  - Alok, Geneva
AU  - Rothman, Joel H
DO  - 10.17912/micropub.biology.000167
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000167/
AB  - The entire C. elegans intestine is derived from a single endodermal progenitor cell (E), the posterior daughter arising from the asymmetric division of the EMS blastomere. During early embryonic development, maternally provided SKN-1/Nrf2 activates the mesendoderm gene regulatory network (GRN) in both E and its sister, MS. A triply redundant Wnt/MAPK/Src signaling system from the neighboring P2 blastomere polarizes EMS, resulting in activation of E fate on the side contacting it. In MS, and in an unsignaled E cell, POP-1/Tcf represses expression of the redundant endoderm specifying factors, the END-1 and -3 GATA-type transcription factors. In a normal E cell, Wnt (initiated by the MOM-2/Wnt ligand) and MAPK signaling (through the MOM-4 MAPKKK) converge on POP-1 to convert it from a repressor to an activator of the end genes which, in collaboration with SKN-1, activates E cell fate (Thorpe et al. 1997; Maduro and Rothman 2002; McGhee 2007; Maduro 2017).
PY  - 2019
JO  - microPublication Biology
ER  -