The electron transport system consists of four complexes that alternatively accept and donate electrons, generating ATP in the process. We have demonstrated previously that the
mev-1 gene encodes one (Cyt-1) of the four subunits (Ip, Cyt-1, Cyt-S and Fp) of complex II.
mev-1 mutants are hypersenstive to oxidative stress and age precociously, particularly at elevated oxygen concentrations. To more systematically explore the consequences of complex II inactivation, we performed RNAi, specifically the soaking method, directed against three of the four subunits of complex II. Embryonic lethality was the predominant result in each case, with hatching reduced by 87%, 75% and 98.3% after functional inactivation of Ip, Cyt-1, and Cyt-S, respectively . The survivors were healthy and not hypersensitive to hyperoxia. The inviable zygotes arrested at various times throughout embryogenesis in proportions specific to the subunit inactivated. For example, Cyt-S inactivation yielded almost 70% inviable zygotes that arrested immediately after fertilization (either prior to nuclear fusion or at the one-cell stage) whereas as almost 60% of Cyt-1-treated embryos reached at least the late morula stage. This embryonic lethality is not surprising given the energy demands throughout embryogenesis.