In multicellular organisms, developmental timing of all types of cells must be well coordinated to achieve organized development of a whole body. Although germ cells differ fundamentally from somatic cells in several aspects, their developmental timing seems well coordinated with that of somatic cells in C. elegans. That is, in N2 hermaphrodites, their proximal germ cells invariably enter meiotic prophase in the L3 stage, develop as sperm in the late L4 stage, switch to differentiate as oocytes immediately after the L4/adult molt, and continue to develop as oocytes throughout the adult stage. Nevertheless, it is not well known whether there exists a mechanism coordinating developmental timing between germline and soma. In our previous RNAi screen of germline-specific cDNAs to identify novel sterile genes, we found RNAi of
asb-1, encoding a germline-specific isoform of mitochondrial ATP synthase b subunit, caused 100% penetrant sterility. As ATP synthase is one of the five complexes of mitochondrial respiratory chain, and defects in some of the genes in the chain, such as
nuo-1,
clk-1, and
atp-2, are known to cause slow growth of worms, we carefully analyzed the time course of
asb-1 germline development through the life. We found in an
asb-1 deletion mutant, its postembryonic germline development was not arrested at any specific stage, but evenly slowed down to twice as slow as that of N2, although the rate of its somatic development was not different from that of N2. As a result, in
asb-1 mutant hermaphrodites, spermatogenesis occurred not in the late L4 stage but 12-24 hours after the L4/adult molt in the adult stage, and oogenesis started not immediately but 48-60 hours after the L4/adult molt in the adult stage, although all
asb-1 mutant sperm and oocytes produced were nonfunctional. Among genes encoding subunits of ATP synthase, we found RNAi of
asg-1, encoding a germline-specific isoform of the g subunit also caused
asb-1-like sterility. On the contrary, we found RNAi of
asb-2 and
asg-2, encoding another isoform of the b and g subunit, respectively, both of which are expressed in the whole body, caused slow growth and larval arrest, as do
nuo-1 and
atp-2. Our results suggest that development of germline is intrinsically independent of that of soma and the timing of germline development is probably determined by its own physiological conditions in which the function of ATP synthase is deeply involved, and that some of its germline-specific components including ASB-1 and ASG-1 function as a booster of germline development to coordinate it with somatic development.