The Key Laboratory of Plant Cell Engineering and Germplasm Innovation, Ministry of Education, Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Jinan 250100, Shandong, China.
Amino Acids. 2012 Aug;43(2):963-71. doi: 10.1007/s00726-011-1159-9. Epub 2011 Dec 6.
Programmed cell death (PCD) plays an important role in insect midgut remodeling during metamorphosis. Insect midgut PCD is triggered by the steroid hormone 20-hydroxyecdysone (20E) and it is mediated by a series of genes. However, the mechanism by which 20E triggers midgut PCD is still unclear. Here, we report a protein phosphatase 6 (PP6) from Helicoverpa armigera playing roles in midgut PCD. PP6 was expressed in the midgut during larval growth and it is significantly increased during metamorphosis. The increase was proven to be regulated by 20E. The juvenile hormone analog methoprene has no effect on PP6 expression. RNA interference analysis suggests that 20E upregulated the PP6 transcript levels through the ecdysone receptor EcRB1. PP6 knockdown by larval feeding or PP6 dsRNA injection resulted in the repression of the midgut PCD during the metamorphic stage. The mechanism was demonstrated to be through the suppression of genes such as Broad (Br), E74a, E75b, HR3, E93, rpr, and caspase, which are involved in 20E signaling pathway or midgut PCD. These findings suggest that PP6 is involved in the 20E signal transduction pathway and participates in the PCD in midgut.
程序性细胞死亡（PCD）在昆虫变态期间中肠重塑中起着重要作用。昆虫中肠 PCD 是由类固醇激素 20-羟基蜕皮酮（20E）触发的，它是由一系列基因介导的。然而，20E 触发中肠 PCD 的机制尚不清楚。在这里，我们报道了来自棉铃虫的一种蛋白磷酸酶 6（PP6）在中肠 PCD 中发挥作用。PP6 在幼虫生长期间在中肠中表达，并且在变态期间显著增加。证明这种增加受到 20E 的调节。保幼激素类似物灭幼脲对 PP6 表达没有影响。RNA 干扰分析表明，20E 通过蜕皮激素受体 EcRB1 上调 PP6 的转录水平。幼虫摄食或注射 PP6 dsRNA 导致变态期的中肠 PCD 受到抑制。该机制是通过抑制参与 20E 信号通路或中肠 PCD 的基因，如 Broad（Br）、E74a、E75b、HR3、E93、rpr 和 caspase 来实现的。这些发现表明 PP6 参与 20E 信号转导途径，并参与中肠的 PCD。
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