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We performed a genetic screen for genes that regulate TORC1, a conserved nutrient signaling pathway in eukaryotes. A yeast screen for synthetic lethality involving a mutation in a member of the ras GTPase family identified a mutant allele of the yeast gene SPAC3G10.05c, encoding an uncharacterized protein. Co-immunoprecipitation experiments showed that Spc3p interacts with RAS2, a negative regulator of TORC1. Mutations in SPAC3G10.05c had no discernible effects on growth on media containing glycerol or methionine. In contrast, these mutant cells showed increased sensitivity to rapamycin, an allosteric inhibitor of TORC1. The TORC1-dependent activation of a reporter gene in vivo was inhibited in spc3Δ cells, but not in the corresponding ras2Δ mutant, providing genetic evidence for an interaction between Spc3p and RAS2 in the activation of TORC1. The rapamycin sensitivity of spc3Δ cells could be suppressed by overexpression of RAS2 but not of RAS2 (148V), a mutant defective in negative regulation of TORC1. Thus, Spc3p plays a novel role in the regulation of TORC1 by interacting with RAS2.Fetal hemoglobin F level as an indicator of the risk of erythroblastosis fetalis.
We determined the distribution of fetal hemoglobin (Hb F) levels of the cord blood of neonates in a delivery room of a hospital. In cases of erythroblastosis fetalis (EF
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