Senescence-induced cellular reprogramming drives cnidarian whole-body regeneration
Senescence-induced cellular reprogramming drives cnidarian whole-body regeneration
复制标题
衰老诱导的细胞重编程驱动刺胞动物全身再生
DOI：
10.1016/j.celrep.2023.112687
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发表时间：
2023
期刊：
影响因子：
8.8
通讯作者：
Frank, Uri
中科院分区：
文献类型：
--
作者：
Salinas-Saavedra, Miguel;Febrimarsa;Krasovec, Gabriel;Horkan, Helen R.;Baxevanis, Andreas D.;Frank, Uri
细胞命运的稳定性对于维持复杂动物的“法律和秩序”至关重要。然而，高稳定性的代价是塑性降低，进而是再生能力差。这种进化的权衡导致了大多数现代动物要么是简单的和可再生的，要么是复杂的和不可再生的。介导细胞可塑性和允许再生的机制仍然未知。我们表明，衰老细胞发出的信号可以破坏邻近体细胞的分化状态，将它们重新编程为能够驱动刺胞水螅共生体全身再生的干细胞。衰老的药理学或遗传学抑制阻止了重编程和再生。相反，在再生环境中诱导短暂的异位衰老导致额外的干细胞和更快的再生。我们认为衰老信号是一个古老的机制，介导细胞的可塑性。了解促进细胞重编程的衰老环境可以提供一种增强再生的途径。
Cell fate stability is essential to maintaining "law and order" in complex animals. However, high stability comes at the cost of reduced plasticity and, by extension, poor regenerative ability. This evolutionary trade-off has resulted in most modern animals being rather simple and regenerative or complex and non-regenerative. The mechanisms mediating cellular plasticity and allowing for regeneration remain unknown. We show that signals emitted by senescent cells can destabilize the differentiated state of neighboring somatic cells, reprogramming them into stem cells that are capable of driving whole-body regeneration in the cnidarianHydractinia symbiolongicarpus. Pharmacological or genetic inhibition of senescence prevents reprogramming and regeneration. Conversely, induction of transient ectopic senescence in a regenerative context results in supernumerary stem cells and faster regeneration. We propose that senescence signaling is an ancient mechanism mediating cellular plasticity. Understanding the senescence environment that promotes cellular reprogramming could provide an avenue to enhance regeneration.
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