SCH9, a putative protein kinase from Saccharomyces cerevisiae, affects HOT1-stimulated recombination

Molecular Genetics and Genomics : MGG
R Prusty, R L Keil

Abstract

HOT1 is a mitotic recombination hotspot derived from yeast rDNA. To further study HOT1 function, trans-acting H OT1 recombination mutants (hrm) that alter hotspot activity were isolated. hrm2-1 mutants have decreased HOT1 activity and grow slowly. The HRM2 gene was cloned and found to be identical to SCH9, a gene that affects a growth-control mechanism that is partially redundant with the cAMP-dependent protein kinase A (PKA) pathway. Deletion of SCH9 decreases HOT1 and rDNA recombination but not other mitotic exchange. Although high levels of RNA polymerase I transcription initiated at HOT1 are required for its recombination-stimulating activity, sch9 mutations do not affect transcription initiated within HOT1. Thus, transcription is necessary but not sufficient for HOT1 activity. TPK1, which encodes a catalytic subunit of PKA, is a multicopy suppressor of the recombination and growth defects of sch9 mutants, suggesting that increased PKA activity compensates for SCH9 loss. RAS2( val19), which codes for a hyperactive RAS protein and increases PKA activity, suppresses both phenotypic defects of sch9 mutants. In contrast to TPK1 and RAS2(val19), the gene for split zinc finger protein 1 (SFP1) on a multicopy vector suppresses onl...Continue Reading

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Citations

May 1, 2012·Nucleic Acids Research·Fernando Gómez-HerrerosSebastián Chávez
Jul 29, 2006·Cell·Valter D Longo, Brian K Kennedy
Jul 10, 2012·Cell Metabolism·Valter D LongoBrian Kennedy
May 22, 2007·Ageing Research Reviews·Matt Kaeberlein, R Wilson Powers
May 4, 2005·Yeast
Apr 27, 2021·G3 : Genes - Genomes - Genetics·Patricia P Peterson, Zhengchang Liu

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