Loukin Stephen, Zhou Xinliang, Kung Ching, Saimi Yoshiro
Laboratory of Molecular Biology, University of Wisconsin-Madison, Madison, WI 53706, USA.
FASEB J. 2008 Jul;22(7):2405-15. doi: 10.1096/fj.07-101410. Epub 2008 Mar 6.
In yeast, osmotic upshock causes a release of vacuolar Ca(2+) through the mechanosensitive transient receptor potential channel, Yvc1. We screened the collection of 4810 yeast gene deletants twice for alterations in this response in an attempt to find elements that regulate the amount of vacuolar Ca(2+) or the Yvc1 channel. Severe overresponders and underresponders to upshock were further scrutinized for their calcium content with (45)Ca and their Yvc1 electrophysiological activities under patch-clamp. The severe underresponders have lower calcium content but no change in Yvc1 activity. The strong overresponders, most of which are deleted of genes involved in cell wall metabolism, have higher calcium content. Wall mutations are known to up-regulate Ca(2+)-calcineurin-dependent genes. It appears that stress on the cell wall induces Ca(2+) accumulation, adaptively anticipating the need in defense or repair against future stress, including osmotic stress.
在酵母中，渗透压骤升会导致液泡中的Ca(2+)通过机械敏感的瞬时受体电位通道Yvc1释放。我们对4810个酵母基因缺失突变体库进行了两轮筛选，以寻找调节液泡Ca(2+)含量或Yvc1通道的元件。对渗透压骤升反应严重过度和反应不足的突变体，进一步通过(45)Ca检测其钙含量，并在膜片钳下检测其Yvc1电生理活性。反应严重不足的突变体钙含量较低，但Yvc1活性没有变化。反应强烈过度的突变体，其中大多数缺失了参与细胞壁代谢的基因，钙含量较高。已知细胞壁突变会上调Ca(2+)-钙调神经磷酸酶依赖性基因。似乎细胞壁上的应激会诱导Ca(2+)积累，从而适应性地预测未来应激（包括渗透压应激）防御或修复的需求。
