The cAMP-dependent protein kinase Pka1 is known as a regulator of glycogenesis, transition into meiosis, proper chromosome segregation, and stress responses in Schizosaccharomyces pombe. We demonstrated that both the cAMP/PKA pathway and glucose limitation play roles in appropriate spindle formation. Overexpression of Mal3 (1–308), an EB1 family protein, caused growth defects, increased 4C DNA content, and induced monopolar spindle formation. Overproduction of a high-affinity microtubule binding mutant (Q89R) and a recombinant protein possessing the CH and EB1 domains (1–241) both resulted in more severe phenotypes than Mal3 (1–308). Loss of functional Pka1 and glucose limitation rescued the phenotypes of Mal3-overexpressing cells, whereas deletion of Tor1 or Ssp2 did not. Growth defects and monopolar spindle formation in a kinesin-5 mutant, cut7-446, was partially rescued by pka1 deletion or glucose limitation. These findings suggest that Pka1 and glucose limitation regulate proper spindle formation in Mal3-overexpressing cells and the cut7-446 mutant.

依赖cAMP的蛋白激酶Pka1被认为是粟酒裂殖酵母（Schizosaccharomyces pombe）中糖原生成，减数分裂过渡，适当的染色体分离和应激反应的调节剂。。我们证明了cAMP / PKA途径和葡萄糖限制均在适当的纺锤体形成中起作用。EB1家族蛋白Mal3（1–308）的过表达导致生长缺陷，4C DNA含量增加和诱导单极纺锤体形成。高亲和力的微管结合突变体（Q89R）和具有CH和EB1结构域的重组蛋白（1-241）的过量生产均导致比Mal3（1-308）更严重的表型。功能性Pka1的丧失和葡萄糖限制挽救了Mal3过表达细胞的表型，而Tor1或Ssp2的缺失则没有。生长缺陷，并在驱动蛋白5突变体，单极纺锤体形成cut7-446，部分被救出pKa1的缺失或葡萄糖限制。这些发现表明Pka1和葡萄糖限制调节过表达Mal3的细胞和cut7-446突变体中适当的纺锤体形成。