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The inactivity of Ure2p, caused by either a ure2 mutation or the presence of the [URE3] prion, increases DAL5 transcription and thus enables Saccharomyces cerevisiae to take up ureidosuccinate (USA+). Rtg2p regulates transcription of glutamate-repressible genes by facilitation of the nuclear entry of the Rtg1 and Rtg3 proteins. We find that rtg2[DELTA] cells take up USA even without the presence of [URE3]. Thus, the USA+ phenotype of rtg2[DELTA] strains is not the result generation of the [URE3] prion but is a regulatory effect. Because rtg1[DELTA] or rtg3[DELTA] mutations or the presence of glutamate do not produce the USA+ phenotype, this is a novel function of Rtg2p. The USA+ phenotype of rtg2[DELTA] strains depends on GLN3, is caused by overexpression of DAL5, and is blocked by mks1[DELTA], but not by overexpression of Ure2p. These characteristics suggest that Rtg2p acts in the upstream part of the nitrogen catabolism regulation pathway. retrograde signaling | DAL5 | [URE3] | prion

CDC7 is an essential gene required for DNA replication in Saccharomyces cerevisiae. Cdc7p homologs have recently been identified in vertebrates, but their role in DNA replication has not yet been addressed. Here we show that antibodies to the Xenopus laevis homolog, xCdc7, interfere with DNA replication in vivo in developing embryos and in vitro in cycling egg extracts. We also demonstrate cell cycle-dependent association of xCdc7 with the Mcm complex, which binds to replication origins and also is required for DNA synthesis. Taken together, these data indicate that the function of xCdc7 is conserved from fungi to vertebrates. xCdc7 protein accumulates after stimulation of resting oocytes with progesterone, suggesting a molecular explanation for previous observations that the development of the capacity for DNA replication requires protein synthesis late in meiosis I.