Toll signalling promotes blastema cell proliferation during cricket leg regeneration via insect macrophages
Toll signalling promotes blastema cell proliferation during cricket leg regeneration via insect macrophages
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DOI：
10.1242/dev.199916
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发表时间：
2022-04-01
期刊：
影响因子：
4.6
通讯作者：
Ohuchi, Hideyo
中科院分区：
文献类型：
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作者：
Bando, Tetsuya;Okumura, Misa;Ohuchi, Hideyo
与人类组织有限的再生能力相比，半代谢昆虫，如两点蟋蟀，可以恢复丢失的组织。板球腿截肢后，伤口表面被伤口表皮覆盖，浆细胞在伤口处聚集，浆细胞是昆虫的巨噬细胞。在这里，我们研究了通过比较RNA测序确定的Toll相关分子在腿部再生中的功能。在灰熊基因组的11个Toll基因中，Toll2-1、Toll2-2和Toll2-5基因在再生过程中表达上调。Toll、Toll2-1、Toll2-2、Toll2-3或Toll2-4的RNA干扰(RNAi)使50%以上的蟋蟀产生再生缺陷。Toll2-2的RNA干扰导致S期细胞和M期细胞比例降低，JAK/STAT信号基因表达减少，浆细胞在胚泡中的积聚减少。使用氯屈膦酸盐去除蟋蟀体内的浆细胞也会产生再生缺陷，再生腿中的增殖细胞也会减少。浆细胞耗竭还下调了再生腿中Toll和JAK/STAT信号基因的表达。这些结果表明，浆细胞中与SPZ-Toll相关的信号通过调节UPD-JAK/STAT信号通路，通过胚泡细胞增殖促进小腿再生。
Hemimetabolous insects, such as the two-spotted cricket Gryllus bimaculatus, can recover lost tissues, in contrast to the limited regenerative abilities of human tissues. Following cricket leg amputation, the wound surface is covered by the wound epidermis, and plasmatocytes, which are insect macrophages, accumulate in the wound region. Here, we studied the function of Toll-related molecules identified by comparative RNA sequencing during leg regeneration. Of the 11 Toll genes in the Gryllus genome, expression of Toll2-1, Toll2-2 and Toll2-5 was upregulated during regeneration. RNA interference (RNAi) of Toll, Toll2-1, Toll2-2, Toll2-3 or Toll2-4 produced regeneration defects in more than 50% of crickets. RNAi of Toll2-2 led to a decrease in the ratio of S- and M-phase cells, reduced expression of JAK/STAT signalling genes, and reduced accumulation of plasmatocytes in the blastema. Depletion of plasmatocytes in crickets using clodronate also produced regeneration defects, as well as fewer proliferating cells in the regenerating legs. Plasmatocyte depletion also downregulated the expression of Toll and JAK/STAT signalling genes in the regenerating legs. These results suggest that Spz-Toll-related signalling in plasmatocytes promotes leg regeneration through blastema cell proliferation by regulating the Upd-JAK/STAT signalling pathway.