METACASPASE9 modulates autophagy to confine cell death to the target cells during Arabidopsis vascular xylem differentiation.
METACASPASE9 modulates autophagy to confine cell death to the target cells during Arabidopsis vascular xylem differentiation.
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DOI：
10.1242/bio.015529
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发表时间：
2016-01-06
期刊：
影响因子：
2.4
通讯作者：
Tuominen H
中科院分区：
文献类型：
--
作者：
Escamez S;André D;Zhang B;Bollhöner B;Pesquet E;Tuominen H
我们发现植物细胞发生程序性细胞死亡的自噬水平决定了周围细胞的命运。我们的方法包括使用能够分化为两种不同细胞类型的拟南芥细胞培养物：经历程序性细胞死亡（PCD）和原生质体自溶的血管管状细胞（TEs）和仍然存活的实质非te。当使用RNAi （MC9-RNAi）降低TE特异性METACASPASE9 （MC9）的表达时，TE细胞类型显示出更高水平的自噬。MC9-RNAi te中自噬的错误调节与非te的异位死亡相吻合，这意味着存在自噬依赖的细胞间信号，从te内部到非te。当AUTOPHAGY2 （ATG2）在MC9-RNAi TEs中特异性下调时，非TEs的活力得以恢复，这表明自噬在细胞死亡的空间限制中的重要性。我们的研究结果表明，其他经历PCD的真核细胞可能也需要严格调节其自噬水平，以避免对周围细胞造成有害后果。摘要：在模拟拟南芥木质部分化的细胞培养中，METACASPASE9调节程序性细胞死亡期间的自噬水平，以防止周围细胞的异位死亡。
We uncovered that the level of autophagy in plant cells undergoing programmed cell death determines the fate of the surrounding cells. Our approach consisted of using Arabidopsis thaliana cell cultures capable of differentiating into two different cell types: vascular tracheary elements (TEs) that undergo programmed cell death (PCD) and protoplast autolysis, and parenchymatic non-TEs that remain alive. The TE cell type displayed higher levels of autophagy when expression of the TE-specific METACASPASE9 (MC9) was reduced using RNAi (MC9-RNAi). Misregulation of autophagy in the MC9-RNAi TEs coincided with ectopic death of the non-TEs, implying the existence of an autophagy-dependent intercellular signalling from within the TEs towards the non-TEs. Viability of the non-TEs was restored when AUTOPHAGY2 (ATG2) was downregulated specifically in MC9-RNAi TEs, demonstrating the importance of autophagy in the spatial confinement of cell death. Our results suggest that other eukaryotic cells undergoing PCD might also need to tightly regulate their level of autophagy to avoid detrimental consequences for the surrounding cells. Summary: In cell cultures that simulate Arabidopsis xylem differentiation, METACASPASE9 modulates the level of autophagy during programmed cell death to prevent ectopic death of the surrounding cells.