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Development 129, 5171-5180 (2002)
Copyright © 2002 The Company of Biologists Limited

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

Kyunghee Koh1,*, Sara M. Peyrot2, Cricket G. Wood1, Javier A. Wagmaister2, Morris F. Maduro1, David M. Eisenmann2 and Joel H. Rothman1,{dagger}

1 Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, CA 93106, USA
2 Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, MD 21250, USA
* Present address: Department of Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA

{dagger} Author for correspondence (e-mail: rothman{at}lifesci.ucsb.edu)

Accepted 9 August 2002

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.

Key words: Cell fusion, Vulva, GATA factor, Hox, C. elegans






© The Company of Biologists Ltd 2002