Huh Gyung-Hye, Damsz Barbara, Matsumoto Tracie K, Reddy Muppala P, Rus Ana M, Ibeas José I, Narasimhan Meena L, Bressan Ray A, Hasegawa Paul M
Center for Plant Environmental Stress Physiology, Purdue University, 1165 Horticulture Building, West Lafayette, IN 47907-1165, USA.
Plant J. 2002 Mar;29(5):649-59. doi: 10.1046/j.0960-7412.2001.01247.x.
Programmed cell death (PCD) is a fundamental cellular process conserved in metazoans, plants and yeast. Evidence is presented that salt induces PCD in yeast and plants because of an ionic, rather than osmotic, etiology. In yeast, NaCl inhibited growth and caused a time-dependent reduction in viability that was preceded by DNA fragmentation. NaCl also induced the cytological hallmarks of lysigenous-type PCD, including nuclear fragmentation, vacuolation and lysis. The human anti-apoptotic protein Bcl-2 increased salt tolerance of wild-type yeast strain and calcineurin-deficient yeast mutant (cnb1Delta) that is defective for ion homeostasis, but had no effect on the NaCl or sorbitol sensitivity of the osmotic hypersensitive hog1Delta mutant -- results that further link PCD in the response to the ion disequilibrium under salt stress. Bcl-2 suppression of cnb1Delta salt sensitivity was ENA1 (P-type ATPase gene)-dependent, due in part to transcriptional activation. Salt-induced PCD (TUNEL staining and DNA laddering) in primary roots of both Arabidopsis thaliana wild type (Col-1 gl1) and sos1 (salt overly sensitive) mutant seedlings correlated positively with treatment lethality. Wild-type plants survived salt stress levels that were lethal to sos1 plants because secondary roots were produced from the shoot/root transition zone. PCD-mediated elimination of the primary root in response to salt shock appears to be an adaptive mechanism that facilitates the production of roots more able to cope with a saline environment. Both salt-sensitive mutants of yeast (cnb1Delta) and Arabidopsis (sos1) exhibit substantially more profound PCD symptoms, indicating that salt-induced PCD is mediated by ion disequilibrium.
程序性细胞死亡（PCD）是后生动物、植物和酵母中保守的基本细胞过程。有证据表明，盐因离子而非渗透病因诱导酵母和植物中的PCD。在酵母中，NaCl抑制生长并导致活力随时间下降，这之前伴随着DNA片段化。NaCl还诱导了溶生性PCD的细胞学特征，包括核碎片化、液泡化和裂解。人类抗凋亡蛋白Bcl-2提高了野生型酵母菌株和离子稳态有缺陷的钙调神经磷酸酶缺陷型酵母突变体（cnb1Delta）的耐盐性，但对渗透超敏hog1Delta突变体的NaCl或山梨醇敏感性没有影响——这些结果进一步将盐胁迫下对离子失衡反应中的PCD联系起来。Bcl-2对cnb1Delta盐敏感性的抑制是依赖ENA1（P型ATP酶基因）的，部分归因于转录激活。盐诱导的拟南芥野生型（Col-1 gl1）和sos1（盐过度敏感）突变体幼苗主根中的PCD（TUNEL染色和DNA梯状条带）与处理致死率呈正相关。野生型植物在对sos1植物致死的盐胁迫水平下存活，因为从茎/根过渡区产生了次生根。PCD介导的对盐冲击的主根消除似乎是一种适应性机制，有助于产生更能应对盐环境的根。酵母（cnb1Delta）和拟南芥（sos1）的盐敏感突变体都表现出更严重的PCD症状，表明盐诱导的PCD是由离子失衡介导的。
