Cell death-induced regeneration in wing imaginal discs requires JNK signalling
Cell death-induced regeneration in wing imaginal discs requires JNK signalling
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DOI：
10.1242/dev.045559
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发表时间：
2010-04-01
期刊：
影响因子：
4.6
通讯作者：
Serras, Florenci
中科院分区：
文献类型：
--
作者：
Bergantinos, Cora;Corominas, Montserrat;Serras, Florenci
再生和组织修复可以替换受损或丢失的身体部位。果蝇成虫盘损伤或破碎后，再生导致正常成虫结构的发育。这个过程可能涉及细胞重排和代偿性增殖的组合。然而，这些过程背后的详细机制知之甚少。我们已经建立了一个系统，允许暂时限制诱导原位细胞死亡。使用Gal 4/Gal 80和UAS-rpr结构，可以进行椎间盘区域的靶向消融并监测再生，而不需要显微外科操作。使用ptc-Gal 4构建体来驱动翼盘中的rpr表达，导致前后边界两侧的前室中的死细胞条纹，而sal-Gal 4驱动器产生包括前细胞和后细胞的死结构域。在这些条件下，再生组织来自受损的隔室，表明隔室限制在再生过程中被保留。我们的研究表明，在再生过程中，活细胞接壤的域中，细胞死亡诱导首先显示细胞骨架重组和顶端到基底关闭的上皮。然后，在伤口附近局部开始增殖，随后在受影响的隔室中更广泛地增殖。最后，我们表明，基因消融组织的再生需要JNK活性。在细胞死亡诱导的再生过程中，JNK途径在愈合组织的前缘而不是在凋亡细胞中被激活，并且是愈合和再生生长的调节所需的。
Regeneration and tissue repair allow damaged or lost body parts to be replaced. After injury or fragmentation of Drosophila imaginal discs, regeneration leads to the development of normal adult structures. This process is likely to involve a combination of cell rearrangement and compensatory proliferation. However, the detailed mechanisms underlying these processes are poorly understood. We have established a system to allow temporally restricted induction of cell death in situ. Using Gal4/Gal80 and UAS-rpr constructs, targeted ablation of a region of the disc could be performed and regeneration monitored without the requirement for microsurgical manipulation. Using a ptc-Gal4 construct to drive rpr expression in the wing disc resulted in a stripe of dead cells in the anterior compartment flanking the anteroposterior boundary, whereas a sal-Gal4 driver generated a dead domain that includes both anterior and posterior cells. Under these conditions, regenerated tissues were derived from the damaged compartment, suggesting that compartment restrictions are preserved during regeneration. Our studies reveal that during regeneration the live cells bordering the domain in which cell death was induced first display cytoskeletal reorganisation and apical-to-basal closure of the epithelium. Then, proliferation begins locally in the vicinity of the wound and later more extensively in the affected compartment. Finally, we show that regeneration of genetically ablated tissue requires JNK activity. During cell death-induced regeneration, the JNK pathway is activated at the leading edges of healing tissue and not in the apoptotic cells, and is required for the regulation of healing and regenerative growth.