Funakoshi T, Matsuura A, Noda T, Ohsumi Y
National Institute for Basic Biology, Myodaijicho, Okazaki, Japan.
Gene. 1997 Jun 19;192(2):207-13. doi: 10.1016/s0378-1119(97)00031-0.
We have isolated 14 apg mutants defective in autophagy in yeast Saccharomyces cerevisiae (Tsukada and Ohsumi, 1993). Among them, APG1 encodes a novel Ser/Thr protein kinase whose kinase activity is essential for autophagy. In the course of searching for genes that genetically interact with APG1, we found that overexpression of APG1 under control of the GAL1 promoter suppressed the autophagy-defective phenotype of apg13-1 mutant. Cloning and sequencing analysis showed that the APG13 gene encodes a novel hydrophilic protein of 738 amino acid residues. APG13 gene is constitutively expressed bot not starvation-inducible. Though dispensable for cell proliferation, APG13 is important for maintenance of cell viability under starvation conditions. apg13 disruptants were defective in autophagy like apg13-1 mutants. Morphological and biochemical investigation showed that a defect in autophagy of delta apg13 was also suppressed by APG1 overexpression. These results imply genetic interaction between APG1 and APG13.
我们已经在酿酒酵母中分离出14个自噬缺陷型的apg突变体(Tsukada和Ohsumi,1993)。其中,APG1编码一种新型的丝氨酸/苏氨酸蛋白激酶,其激酶活性对于自噬至关重要。在寻找与APG1发生遗传相互作用的基因的过程中,我们发现,在GAL1启动子控制下APG1的过表达抑制了apg13-1突变体的自噬缺陷表型。克隆和测序分析表明,APG13基因编码一种由738个氨基酸残基组成的新型亲水性蛋白。APG13基因组成型表达,而非饥饿诱导型表达。虽然APG13对于细胞增殖并非必需,但对于在饥饿条件下维持细胞活力很重要。apg13缺失突变体与apg13-1突变体一样存在自噬缺陷。形态学和生化研究表明,APG1的过表达也抑制了δapg13自噬缺陷。这些结果暗示了APG1与APG13之间的遗传相互作用。