Loss-of-function mutations in
gon-2 have a partial maternal effect, causing a severe reduction in gonadal cell divisions. In the most extreme cases, none of the gonadal progenitor cells divide. In less severe cases, Z1 and/or Z4 execute incomplete gonadal lineages, often failing to initiate divisions until the second larval stage. The divisions of the germline precursors, Z2 and Z3, are also affected; however this is probably a consequence of the defects in somatic cell fates. Thanks to assistance from the Genome Project, we have established that
gon-2 is most likely to encode a large multipass transmembrane protein (T01H8.5) that has similarity to the Drosophila Trp ion channel. Fusion constructs that carry the T01H8.5 genomic region downstream of a heatshock promoter are capable of rescuing
gon-2(
q388) in a heatshock-dependent manner. We are in the process of sequencing mutant alleles to further verify the molecular identity of
gon-2, and have begun the sequencing of cDNAs to confirm the locations of the intron/exon boundaries predicted by GeneFinder. At least five other Trp-related coding sequences are present in the C. elegans genome (Coulson et al., in progress; Colbert, Smith and Bargmann; WCWM #160). Therefore,
gon-2 could produce a tissue-specific Trp protein, or it could be broadly expressed, but non-essential in extra-gonadal tissues. We are currently assembling fusion constructs that will enable us to examine the spatial and temporal expression patterns of
gon-2. Suppressor/enhancer screens are also underway in an attempt to identify genes that interact with
gon-2 to control gonadal cell divisions.