We have performed systematic RNAi screening and identified genes that cause sterility but no obvious somatic phenotypes. Among such genes is
hmg-3, which encodes a homolog of human HMG-box protein SSRP1 (Structure Specific Recognition Protein 1). SSRP1 is known to be involved in various processes such as elongation of transcripts, DNA replication, and transcriptional regulation of specific genes. RNAi against
hmg-3 resulted in sterile F1 progeny with an underproliferated germline. We produced an
hmg-3 deletion mutant, which was zygotically sterile showing a nearly identical phenotype to
hmg-3(RNAi) F1 worms. In germline development, a defect in
glp-1 results in generation of fewer germ cells. However, the
glp-1 defect cannot suppress tumorigenesis of the
gld-1gld-2 double mutant, suggesting that
glp-1 functions upstream of
gld-1 and
gld-2. To explore the possibility that
hmg-3 is involved in
glp-1 pathway, we performed RNAi against
hmg-3 in the
gld-1(
q485)
gld-2(
q497) mutant. The number of germ cells in the resulting
hmg-3(RNAi) strain was apparently fewer than that in the untreated strain, although it was still greater than that in
hmg-3(RNAi) F1 animals derived from the wild-type strain. These results suggest that
hmg-3 may have some role in the
glp-1 pathway. The
hmg-3 gene has one paralog,
hmg-4. Unlike
hmg-3(RNAi),
hmg-4(RNAi) caused larval lethality at L1-2 stage. In addition, disruption of both
hmg-3 and
hmg-4 by RNAi resulted in synthetic embryonic lethality. Therefore, these two genes may be functionally redundant in embryogenesis, and they may function independently in germ and soma after embryogenesis. To investigate whether a similar mechanism is conserved in another worm species, we cloned C. briggsae homologs of
hmg-3 and
hmg-4, namely
Cb-hmg-3 and
Cb-hmg-4, and analysed their function by RNAi. F1 progeny of
Cb-hmg-3(RNAi) animals showed sterility with almost no obvious somatic defect, as was the case with C. elegans. However, the germline of the sterile adults was not underproliferated but tumorigenic. In contrast, RNAi against
Cb-hmg-4 resulted in only moderate phenotypes, such as smaller body size, showing no significant effect on viability or fertility. Therefore,
Cb-hmg-4 did not seem to be as important as C. elegans
hmg-4. However, disruption of both
Cb-hmg-3 and
Cb-hmg-4 by RNAi resulted in synthetic embryonic lethality. These observations suggest that the basic system that two types of SSRP1 differentiate their function in germ and soma during development is conserved between C. elegans and C. briggsae, although there are some apparent modifications.