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热应激:嗜糖小球藻程序性细胞死亡的诱导因素

Heat stress: an inducer of programmed cell death in Chlorella saccharophila.

作者信息

Zuppini Anna, Andreoli Carlo, Baldan Barbara

机构信息

Dipartimento di Biologia, Università di Padova, via U. Bassi 58/B, 35131 Padova, Italy.

出版信息

Plant Cell Physiol. 2007 Jul;48(7):1000-9. doi: 10.1093/pcp/pcm070. Epub 2007 Jun 13.

Abstract

Programmed cell death (PCD) has been recognized as a fundamental cellular process conserved in metazoans, plants and yeast. However, the cellular mechanisms leading to PCD have not been fully elucidated in unicellular organisms. Evidence is presented that heat stress induces PCD in Chlorella saccharophila cells. Our results demonstrate that heat shock triggers a PCD pathway occurring with characteristics features such as chromatin condensation, DNA fragmentation, cell shrinkage and detachment of the plasma membrane from the cell wall, and suggest the presence of caspase 3-like activity. The caspase 3 inhibitor Ac-DEVD-CHO gave significant protection against heat shock-induced cell death. Moreover, a reduction in photosynthetic pigment contents associated with alteration of chloroplast morphology and a fairly rapid disappearance of the ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit and the light-harvesting complex of PSII have been observed. The timing of events in the signaling cascade associated with the C. saccharophila heat shock PCD response is discussed. Insights into this field may have general implications for understanding the pathway of cell death in unicellular green algae.

摘要

程序性细胞死亡(PCD)已被公认为是后生动物、植物和酵母中保守的基本细胞过程。然而,单细胞生物中导致PCD的细胞机制尚未完全阐明。有证据表明热应激可诱导嗜糖小球藻细胞发生PCD。我们的结果表明,热休克触发了一条具有染色质浓缩、DNA片段化、细胞收缩以及质膜与细胞壁分离等特征的PCD途径,并提示存在类似caspase 3的活性。caspase 3抑制剂Ac-DEVD-CHO对热休克诱导的细胞死亡具有显著的保护作用。此外,还观察到光合色素含量的降低与叶绿体形态的改变以及核酮糖-1,5-二磷酸羧化酶/加氧酶大亚基和PSII捕光复合体的相当快速消失有关。本文讨论了嗜糖小球藻热休克PCD反应相关信号级联中事件发生的时间。对该领域的深入了解可能对理解单细胞绿藻的细胞死亡途径具有普遍意义。

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