摘要 : Staurosporine-induced cell death in Neurospora crassa includes a well defined sequence of alterations in cytosolic calcium levels, comprising extracellular Ca2+ influx and mobilization of Ca2+ from internal stores. Here, we show t... 展开 Staurosporine-induced cell death in Neurospora crassa includes a well defined sequence of alterations in cytosolic calcium levels, comprising extracellular Ca2+ influx and mobilization of Ca2+ from internal stores. Here, we show that cells undergoing respiratory stress due to the lack of certain components of the mitochondrial complex I (like the 51 kDa and 14 kDa subunits) or the Ca2+-binding alternative NADPH dehydrogenase NDE-1 are hypersensitive to staurosporine and incapable of setting up a proper intracellular Ca2+ response. Cells expressing mutant forms of NUO51 that mimic human metabolic diseases also presented Ca2+ signaling deficiencies. Accumulation of reactive oxygen species is increased in cells lacking NDE-1 and seems to be required for Ca2+ oscillations in response to staurosporine. Measurement of the mitochondrial levels of Ca2+ further supported the involvement of these organelles in staurosporine-induced Ca2+ signaling. In summary, our data indicate that staurosporine-induced fungal cell death involves a sophisticated response linking Ca2+ dynamics and bioenergetics. (C) 2015 Elsevier B.V. All rights reserved. 收起