Cell fates and fusion in the C. elegans vulval primordium are regulated by the EGL-18 and ELT-6 GATA factors -- apparent direct targets of the LIN-39 Hox protein.

TitleCell fates and fusion in the C. elegans vulval primordium are regulated by the EGL-18 and ELT-6 GATA factors -- apparent direct targets of the LIN-39 Hox protein.
Publication TypeJournal Article
Year of Publication2002
AuthorsKoh K, Peyrot SM, Wood CG, Wagmaister JA, Maduro MF, Eisenmann DM, Rothman JH
JournalDevelopment
Volume129
Issue22
Pagination5171-80
Date Published2002 Nov
ISSN0950-1991
KeywordsAnimals, Binding Sites, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cell Differentiation, Cell Fusion, Dimerization, DNA-Binding Proteins, Enhancer Elements, Genetic, Female, GATA Transcription Factors, Green Fluorescent Proteins, Helminth Proteins, Homeodomain Proteins, Luminescent Proteins, Mutation, Neurons, Recombinant Proteins, Transcription Factors, Vulva
Abstract

Development of the vulva in C. elegans is mediated by the combinatorial action of several convergent regulatory inputs, three of which, the Ras, Wnt and Rb-related pathways, act by regulating expression of the lin-39 Hox gene. LIN-39 specifies cell fates and regulates cell fusion in the mid-body region, leading to formation of the vulva. In the lateral seam epidermis, differentiation and cell fusion have been shown to be regulated by two GATA-type transcription factors, ELT-5 and -6. We report that ELT-5 is encoded by the egl-18 gene, which was previously shown to promote formation of a functional vulva. Furthermore, we find that EGL-18 (ELT-5), and its paralogue ELT-6, are redundantly required to regulate cell fates and fusion in the vulval primordium and are essential to form a vulva. Elimination of egl-18 and elt-6 activity results in arrest by the first larval stage; however, in animals rescued for this larval lethality by expression of ELT-6 in non-vulval cells, the post-embryonic cells (P3.p-P8.p) that normally become vulval precursor cells often fuse with the surrounding epidermal syncytium or undergo fewer than normal cell divisions, reminiscent of lin-39 mutants. Moreover, egl-18/elt-6 reporter gene expression in the developing vulva is attenuated in lin-39(rf) mutants, and overexpression of egl-18 can partially rescue the vulval defects caused by reduced lin-39 activity. LIN-39/CEH-20 heterodimers bind two consensus HOX/PBC sites in a vulval enhancer region of egl-18/elt-6, one of which is essential for vulval expression of egl-18/elt-6 reporter constructs. These findings demonstrate that the EGL-18 and ELT-6 GATA factors are essential, genetically redundant regulators of cell fates and fusion in the developing vulva and are apparent direct transcriptional targets of the LIN-39 Hox protein.

Alternate JournalDevelopment
PubMed ID12399309
Grant ListHD37487 / HD / NICHD NIH HHS / United States