玉米小球腔菌 Race T 毒素诱导 T 细胞质玉米线粒体 NAD 渗漏。
Helminthosporium maydis Race T Toxin Induces Leakage of NAD from T Cytoplasm Corn Mitochondria.
机构信息
Department of Plant Breeding and Biometry, Cornell University, Ithaca, New York 14853.
出版信息
Plant Physiol. 1979 Jun;63(6):1149-53. doi: 10.1104/pp.63.6.1149.
Abstract
The mechanism by which Helminthosporium maydis race T toxin inhibits respiration dependent on NAD(+)-linked substrates in T cytoplasm corn mitochondria was investigated. The toxin did not cause leakage of the soluble matrix enzyme malate dehydrogenase from the mitochondria or inhibit malate dehydrogenase or isocitrate dehydrogenase directly. The toxin did increase the permeability of the inner membranes of T cytoplasm, but not N cytoplasm, mitochondria to NAD(+). Added NAD(+) partially or fully restored toxin-inhibited electron transport in T cytoplasm mitochondria. Thiamin pyrophosphate had a similar effect when malate was the substrate. It was concluded that the inhibition of respiration of NAD(+)-linked substrates by the toxin is due to depletion of the intramitochondrial pool of NAD(+) and other coenzymes.
摘要
研究了玉米细胞质线粒体中依赖 NAD(+)连接底物的呼吸被 Helminthosporium maydis race T 毒素抑制的机制。该毒素不会导致线粒体可溶性基质酶苹果酸脱氢酶漏出，也不会直接抑制苹果酸脱氢酶或异柠檬酸脱氢酶。毒素确实增加了 T 细胞质但不是 N 细胞质线粒体内膜对 NAD(+)的通透性。添加 NAD(+)部分或完全恢复了 T 细胞质线粒体中毒素抑制的电子传递。当苹果酸作为底物时，焦磷酸硫胺素也有类似的效果。结论是，毒素对 NAD(+)连接底物呼吸的抑制是由于线粒体中 NAD(+)和其他辅酶池的耗竭所致。
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