细胞的程序性死亡是由基因控制的生物学事件，它在生物发育和维持机体内环境稳定的过程中有重要意义。最常见的程序性死亡是细胞凋亡，凋亡的过程会伴随着一系列细胞形态改变和生化标志。
以往对凋亡的研究都是针对真核细胞的，而本文的研究者发现，在抗生素压力下，大肠杆菌也会显示出凋亡的特殊标记。包括细胞膜内侧的磷脂酰丝氨酸外翻、染色质凝集和DNA断裂等。通过蛋白质组学和基因组学分析，研究人员发现多能性因子RecA是诱导这些凋亡表型的关键因子。RecA能够结合多肽序列，并将其引导到ClpXP蛋白酶附近，通过ClpXP将其水解。这项研究表明，在原核生物中，或许也有与真核生物控制凋亡相似的机制来标记和去除濒死的细胞。（生物谷 Bioon.com ）
doi:10.1016/j.molcel.2012.04.027
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Antibiotic-Induced Bacterial Cell Death Exhibits Physiological and Biochemical Hallmarks of Apoptosis
Daniel J. Dwyer, Diogo M. Camacho, Michael A. Kohanski, Jarred M. Callura, James J. Collins
Programmed cell death is a gene-directed process involved in the development and homeostasis of multicellular organisms. The most common mode of programmed cell death is apoptosis, which is characterized by a stereotypical set of biochemical and morphological hallmarks. Here we report that Escherichia coli also exhibit characteristic markers of apoptosis—including phosphatidylserine exposure, chromosome condensation, and DNA fragmentation—when faced with cell death-triggering stress, namely bactericidal antibiotic treatment. Notably, we also provide proteomic and genetic evidence for the ability of multifunctional RecA to bind peptide sequences that serve as substrates for eukaryotic caspases, and regulation of this phenotype by the protease, ClpXP, under conditions of cell death. Our findings illustrate that prokaryotic organisms possess mechanisms to dismantle and mark dying cells in response to diverse noxious stimuli and suggest that elaborate, multilayered proteolytic regulation of these features may have evolved in eukaryotes to harness and exploit their deadly potential.
