基因在结合之前起作用,为Saccharomyces cerevisiae核准备卡里奥加米
Cell
|May 1, 1983
概括
酵母核基因KAR1,CDC28和CDC37中的突变会在结合过程中破坏核聚变. 它们的基因产物可能在细胞融合之前起作用,在细胞核之间扩散.
科学领域:
- 细胞生物学 细胞生物学
- 遗传学 是一个遗传学.
- 分子生物学分子生物学
背景情况:
- 在Saccharomyces cerevisiae中,核聚变 (核相生) 对于性繁殖至关重要.
- 在KAR1,CDC4,CDC28和CDC37基因中的突变会破坏卡里约加米.
- 这些基因表现出"核优势",需要来自两个母核的功能性等位基因.
研究的目的:
- 为了研究酵母菌的核主导机制.
- 为了确定基因产品是否可以在核之间移动.
- 为了阐明基因产品相对于细胞融合的功能时间.
主要方法:
- 检查异质细胞质细胞体内突变细胞核的卡里奥加米能力.
- 分析卡里奥加米缺陷的表型抑制.
主要成果:
- 由kar1,cdc28和cdc37突变引起的卡里奥加米缺陷在核共享异质细胞质时被抑制.
- 这种抑制表明KAR1,CDC28和CDC37基因产物可以在核之间扩散.
- 这些基因产物很可能在细胞融合之前就已经起作用了.
结论:
- KAR1,CDC28和CDC37基因产物是可扩散的,并在细胞融合之前起作用.
- 疾病预防控制中心28和疾病预防控制中心37可能是随后的细胞周期中卡里约加米所需的核结构部件.
- 这表明,在一个细胞周期中,这些蛋白质必须被纳入细胞核的模型,以便在下一个细胞周期中实现成功的肌肉修复.
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