Communication between tissues in an organ system is necessary to co-ordinate their development and to ensure that they function as a unit. The egg-laying system in C . elegans offers a good model system for animal organ development. During the development of the egg-laying system, reciprocal interactions between the somatic gonad and the vulva co-ordinate development between these two tissues. The Anchor Cell (AC) of the somatic gonad initially induces 3 of 6 multipotential Vulval Precursor Cells (VPCs) to form the vulval cells by the LIN-3-LET-23 mediated signaling pathway. Subsequently, some cells of the 1deg VPC lineage reciprocally signal to the uterine cells and induce
uv1 cell fate using LIN-3-LET-23 again. Some genes important for the AC to vulva signal also mediate the vulva to uterus signal, whereas others function in one or the other developmental pathway. For example, only the vulval transcription of
lin-3 requires EGL-38, a PAX transcription factor, while the earlier AC expression is EGL-38 independent (1). EGL-38 is also required for the normal morphology of vulF cells (2). Thus it impacts both the somatic and the vulval cells to co-ordinate the development of the egg-laying system. To investigate the different roles of
egl-38 in the egg-laying system development, we have studied the defects associated with different
egl-38 alleles. We have found that different
egl-38 alleles disrupt the different egg-laying features of egg-laying ability,
lin-3 expression,
uv1 specification and vulF morphology to varying degrees. For example
egl-38(
n578) mutants are defective for all functions,
egl-38(
gu22) mutants are competent for all functions and
egl-38(
sy294) mutants are defective for
lin-3 expression but retain a high level of normal vulF morphogenesis. To identify additional genes that function with
egl-38 , we performed a genetic screen for suppressors of the
egl-38(
n578) egg-laying defect (2, 3). We isolated four suppressor mutations from a screen of about 49,000 haploid genomes. Each suppressor is recessive and maps to LG IV. All four exhibit partial failure to complement in trans to each other. However they correspond to at least two genes since one (
gu68) maps between
unc-24 and
sqv-1 while another (
gu51) maps to the left of
unc-24 between
unc-5 and
lin-33 . Interestingly, these suppressors suppress the 1deg vulval morphological defect and the
uv1 specification defect though they still lack LIN-3 expression. We are currently doing further fine mapping and cosmid rescue experiments to identify the genes. Identification of these suppressor genes along with the characterization of the egg-laying system in the different
egl-38 alleles will enable us to better understand at a molecular and cellular level, the 'crosstalk' occurring between tissues to co-ordinate organ development. (1) Chang, C., Newman, A.P and Sternberg, P.W. (1999) Current Biology 9: 237-246 (2) Chamberlin, H. M., Palmer, R. E., Newman, A. P., et al (1997) Development 124:3919-3928 (3) Trent, C., Tsung, N and Horvitz, H. R. (1983) Genetics 104: 619-647