14
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Dosage suppressors of the dominant G1 cyclin mutant CLN3-2: identification of a yeast gene encoding a putative RNA/ssDNA binding protein.

      Molecular & general genetics : MGG
      Amino Acid Sequence, Cell Division, genetics, Cyclins, DNA, Single-Stranded, metabolism, DNA-Binding Proteins, chemistry, physiology, Fungal Proteins, G1 Phase, Gene Expression Regulation, Fungal, Genes, Dominant, Genes, Fungal, Genes, Suppressor, Genotype, Molecular Sequence Data, Nuclear Proteins, RNA, Fungal, RNA-Binding Proteins, Restriction Mapping, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Sequence Analysis, Transcription, Genetic

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Three G1 cyclins, CLN1, CLN2, and CLN3, have been identified in the budding yeast Saccharomyces cerevisiae. G1 cyclins are essential, albeit functionally redundant, rate-limiting activators of cell cycle initiation. We have isolated dosage-dependent suppressor genes (designated HMD genes) of the mating defect caused by CLN3-2, a dominant mutation in CLN3, HMD2 and HMD3 are identical to STE4 and STE5, respectively, HMD1 is an essential gene that encodes a protein containing a putative RNA binding domain. Overproduction of HMD1 results in a relatively specific reduction in the level of the CLN3 or CLN3-2 transcript. This reduction occurs subsequent to transcription initiation of CLN3 since overexpression of HMD1 did not affect expression of a heterologous transcript from the CLN3 promoter but did result in a reduction of CLN3 transcript expressed from a heterologous promoter. HMD1 has at least one essential role independent of its effect on CLN3 since HMD1 remains essential for viability in the absence of a functional CLN3 gene.

          Related collections

          Author and article information

          Comments

          Comment on this article