sck1, a high copy number suppressor of defects in the cAMP-dependent protein kinase pathway in fission yeast, encodes a protein homologous to the Saccharomyces cerevisiae SCH9 kinase.
sck1, a high copy number suppressor of defects in the cAMP-dependent protein kinase pathway in fission yeast, encodes a protein homologous to the Saccharomyces cerevisiae SCH9 kinase.
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sck1 是裂殖酵母中 cAMP 依赖性蛋白激酶途径缺陷的高拷贝数抑制因子，编码与酿酒酵母 SCH9 激酶同源的蛋白质。
DOI：
10.1093/genetics/140.2.457
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发表时间：
1995
期刊：
影响因子：
3.3
通讯作者：
Hoffman,CS
中科院分区：
文献类型：
--
作者：
Jin,M;Fujita,M;Culley,BM;Apolinario,E;Yamamoto,M;Maundrell,K;Hoffman,CS
粟酒裂殖酵母调节细胞内cAMP水平，从而调节cAMP依赖性蛋白激酶（PKA）活性，以响应营养条件的变化。八个git基因中的任何一个突变都会抑制葡萄糖对fbp1转录的抑制，改变细胞形态，并导致生长速率降低。八个git基因编码腺苷酸环化酶激活途径的组分、腺苷酸环化酶本身和PKA的催化亚基。这些基因中的三个在其他研究中被鉴定为减数分裂的调节因子。在这里，我们证明了sck 1基因（克隆为git 3突变的高拷贝数抑制因子）能够抑制任何这些git基因突变所带来的缺陷。序列分析表明，sck1编码的蛋白质最密切相关的酿酒酵母SCH9蛋白激酶，以前已被确定为高拷贝数的突变抑制S。酿酒酵母，降低或消除PKA活性。sck 1基因的破坏导致退出稳定期的显着延迟时，结合破坏PKA的催化亚基编码的pka 1（git6）基因。然而，sck 1破坏本身对fbp 1转录、减数分裂或退出稳定期的影响很小或没有影响，并且不会增强在pka 1突变体中观察到的组成型fbp 1转录。因此，sck 1似乎在pka 1调节的途径中以冗余的方式发挥作用，但程度不同。
Schizosaccharomyces pombe regulates intracellular cAMP levels, and thus cAMP-dependent protein kinase (PKA) activity, in response to changes in nutrient conditions. Mutations in any of eight git genes inhibit glucose repression of fbp1 transcription, alter the cell morphology, and cause a reduction in the growth rate. The eight git genes encode components of an adenylate cyclase activation pathway, adenylate cyclase itself, and the catalytic subunit of PKA. Three of these genes have been identified in other studies as regulators of meiosis. Here we show that the sck1 gene, cloned as a high copy number suppressor of a mutation in git3, is able to suppress the defects conferred by a mutation in any of these git genes. Sequence analysis suggests that sck1 encodes a protein most closely related to the Saccharomyces cerevisiae SCH9 protein kinase that had previously been identified as a high copy number suppressor of mutations in S. cerevisiae that reduce or eliminate PKA activity. Disruption of the sck1 gene causes a significant delay in exit from stationary phase when combined with a disruption of the pka1 (git6) gene encoding the catalytic subunit of PKA. However, the sck1 disruption by itself has little or no effect upon fbp1 transcription, meiosis, or exit from stationary phase, and does not enhance the constitutive fbp1 transcription observed in a pka1 mutant. Therefore, sck1 appears to function in a redundant fashion to pka1, but to varying degrees, in the pathways regulated by pka1.