A common SSD1 truncation is toxic to cells entering quiescence and promotes sporulation.
A common SSD1 truncation is toxic to cells entering quiescence and promotes sporulation.
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DOI：
10.17912/micropub.biology.000671
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发表时间：
2022
影响因子：
--
通讯作者：
Miles, Shawna
中科院分区：
文献类型：
--
作者：
Breeden, Linda;Miles, Shawna
Ssd 1 p是酿酒酵母中的一种RNA结合蛋白，在细胞分裂、细胞命运决定、应激反应和毒力中起重要作用。实验室菌株W303编码末端截短ssd 1 -2，通常将其解释为功能丧失的等位基因。我们已经证明ssd 1 -2对mpt 5-Δ突变体和进入稳定期和静止期的二倍体是有毒的。ssd 1-Δ null没有显示出毒性，表明ssd 1 -2正在破坏一种不仅仅需要Ssd 1 p的基本功能。ssd 1 -2细胞也比ssd 1-Δ对应激更敏感。这些表型对SSD 1 -1是隐性的。相反，ssd 1 -2在促进产孢中起主导作用。
Ssd1p is an RNA binding protein in Saccharomyces cerevisiae that plays an important role in cell division, cell fate decisions, stress response and virulence. Lab strain W303 encodes the terminal truncation ssd1-2, which is typically interpreted to be a loss of function allele. We have shown that ssd1-2 is toxic to mpt5-Δ mutants and to diploids entering stationary phase and quiescence. The ssd1-Δ null shows no toxicity, indicating that ssd1-2 is disrupting an essential function that does not solely require Ssd1p. ssd1-2 cells are also more sensitive to stress than ssd1-Δ . These phenotypes are recessive to SSD1-1 . In contrast, ssd1-2 plays a dominant role in promoting sporulation.