The <i>SCH9</i> protein kinase mRNA contains a long 5′ leader with a small open reading frame

Blasi, Francesco Di; Carra, Elena; Vendittis, Emmanuele De; Masturzo, Pietro; Burderi, Emanuele; Lambrinoudaki, Ιrene; Mirisola, Mario G.; Seidita, Gregorio; Fasano, Ottavio

doi:10.1002/yea.320090104

Cited by 9 publications

(2 citation statements)

References 36 publications

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“…Previous attempts to identify downstream effectors of the Ras/A kinase pathway have exploited classical and gene dosage (high-copy-number) suppressor analyses (4,9,13,24,30). Two genes exhibiting significant homology to known protein kinase genes were identified in separate selections for suppressors of conditional defects in the A kinase pathway.…”

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confidence: 99%

Suppression of a yeast cyclic AMP-dependent protein kinase defect by overexpression of SOK1, a yeast gene exhibiting sequence similarity to a developmentally regulated mouse gene.

Ward¹,

Garrett²

1994

Mol. Cell. Biol.

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Saccharomyces cerevisiae cyclic AMP-dependent protein kinase (A kinase) activity is essential for growth and cell cycle progression. Dependence on A kinase function can be partially relieved by the inactivation of a second kinase encoded by the gene YAK]. We have isolated two new genes, SOKI and SOK2 (suppressor of kinase), as gene dosage suppressors of the conditional growth defect of several temperature-sensitive A kinase mutants. Overexpression of SOKI, like lesions in YAK], also restores growth to a strain (tpkl tpk2 tpk3) lacking all A kinase activity. The SOKI gene is not essential, but a sokl::HIS3 disruption abrogates suppression of an A kinase defect by yak). These results suggest that Yakl and Sokl define a linear pathway that is partially redundant with that of the A kinase. Activation of Sokl, by SOK1 overexpression or by inactivation of the negative regulator Yakl, renders a cell independent of A kinase function. The implications of such a model are particularly intriguing in light of the nuclear localization pattern of the overexpressed Sokl protein and the primary sequence homology between SOKI and a recently described, developmentally regulated mouse gene.In the yeast Saccharomyces cerevisiae, cyclic AMP (cAMP)-dependent protein kinase (A kinase) activity is essential for growth and cell cycle progression. Cells deficient in this activity stop growing and arrest in G1 in a manner similar to that observed for wild-type cells deprived of nutrients (16,20,21 (919) 684-8598. gets of the yeast A kinase have been described and include proteins involved in processes such as carbohydrate storage and metabolism, phospholipid metabolism, and transcriptional regulation, as well as functions involved in the synthesis and breakdown of cAMP (for reviews, see references 1 and 2). Nevertheless, it remains unclear whether A kinase phosphorylation of these known targets can influence whether the cell exits the cell cycle or continues proliferation (3).Previous attempts to identify downstream effectors of the Ras/A kinase pathway have exploited classical and gene dosage (high-copy-number) suppressor analyses (4, 9, 13, 24, 30). Two genes exhibiting significant homology to known protein kinase genes were identified in separate selections for suppressors of conditional defects in the A kinase pathway. Null mutations of one gene, YAK1, allowed strains completely deficient in A kinase activity to grow; tpkl tpk2 tpk3 YAK1+ strains are inviable, but tpkl tpk2 tpk3 yakl strains grow (13). These and other results led us to propose that Yakl served as a negative regulator of cell growth, in a pathway parallel to that of the A kinase, with overlapping but antagonistic effects (14). The second gene exhibiting protein kinase gene homology, SCH9, was isolated as a high-copy-number suppressor of a temperature-sensitive cdc25(Ts) mutation. Although the mechanism by which Sch9 overproduction alleviates the A kinase defect is not known, the reciprocal suppression of null mutations in both pathways (a tpk strain grows in the ...

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confidence: 99%

Suppression of a yeast cyclic AMP-dependent protein kinase defect by overexpression of SOK1, a yeast gene exhibiting sequence similarity to a developmentally regulated mouse gene.

Ward¹,

Garrett²

1994

Mol. Cell. Biol.

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“…SCH9 is required for TORC1-mediated regulation of ribosome biogenesis, translation initiation, and entry into G 0 phase (di Blasi et al 1993 ;Hay and Sonenberg 2004 ). Sch9p also shows sequence homology to the kinase Akt, a central component of insulin/IGF-1-like signaling pathways (Paradis and Ruvkun 1998 ;Burgering and Coffer 1995 ).…”

Section: Dietary Restriction and Yeast Replicative Lifespanmentioning

confidence: 99%

Aging in the Single-Celled Eukaryote, S. cerevisiae

Kennedy

2015

Stem Cell Aging: Mechanisms, Consequences, Rejuvenation

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In the last few decades, the budding yeast Saccharomyces cerevisiae has emerged as a simple and powerful model organism to study aging. Replicative aging and chronological aging are the two major models that have been established in yeast. In this chapter, we review the two aging model systems, focusing on genes and pathways that modulate replicative and chronological aging. The purpose of this chapter is to provide an overall understanding of the aging process in the single-celled yeast and a basis by which to generate models of molecular mechanisms that may affect aging stem cell populations in adult tissues, as well as the multicellular eukaryotes they inhabit.

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RAS proteins and control of the cell cycle inSaccharomyces cerevisiae

Fasano

1995

Biochemistry of Cell Membranes

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The SCH9 protein kinase mRNA contains a long 5′ leader with a small open reading frame

Cited by 9 publications

References 36 publications

Suppression of a yeast cyclic AMP-dependent protein kinase defect by overexpression of SOK1, a yeast gene exhibiting sequence similarity to a developmentally regulated mouse gene.

Suppression of a yeast cyclic AMP-dependent protein kinase defect by overexpression of SOK1, a yeast gene exhibiting sequence similarity to a developmentally regulated mouse gene.

Aging in the Single-Celled Eukaryote, S. cerevisiae

RAS proteins and control of the cell cycle inSaccharomyces cerevisiae

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