Department of Biology, Colorado State University, Fort Collins, CO 80523, United States of America; Department of Clinical Sciences, Colorado State University, Fort Collins, CO 80523, United States of America.
Department of Biology, Colorado State University, Fort Collins, CO 80523, United States of America.
Comp Biochem Physiol Part D Genomics Proteomics. 2018 Dec;28:37-53. doi: 10.1016/j.cbd.2018.06.001. Epub 2018 Jun 15.
A transcriptome of the Gecarcinus lateralis molting gland (Y-organ or YO) contained 48,590 contiguous sequences (contigs) from intermolt (IM), early premolt (EP), mid premolt (MP), late premolt (LP), and postmolt (PM) stages. The YO is kept in the basal state in IM by molt-inhibiting hormone (MIH)/cyclic nucleotide-dependent signaling. YO activation in EP requires down-regulation of MIH signaling and activation of mechanistic target of rapamycin (mTOR)-dependent protein synthesis. Transition of the YO to the committed state in MP requires activin/transforming growth factor-beta (TGFβ) signaling. YO repression occurs at the end of LP. A total of 28,179 contigs (58%) showed molt stage-specific changes in gene expression. The largest number of differentially-expressed genes (DEGs) were at the IM/EP (16,142 contigs), LP/PM (18,161 contigs), and PM/IM (8290 contigs) transitions. By contrast, the numbers of DEGs were 372 and 1502 contigs for the EP/MP and MP/LP transitions, respectively. DEG analysis of 23 signal transduction pathways showed significant changes in MIH, mTOR, activin/TGFβ, Notch, MAP kinase, and Wnt signaling. Down-regulation of MIH signaling genes in premolt is consistent with reduced MIH sensitivity in MP and LP. Up-regulation of mTOR signaling genes in IM and premolt stages is consistent with its role in YO activation and sustained ecdysteroidogenesis. Up-regulation of activin/TGFβ signaling genes in EP and MP is consistent with the role of a myostatin/activin-like factor in YO commitment. Notch, MAP kinase, and Wnt DEG analysis may indicate possible crosstalk with the MIH, mTOR, and activin/TGFβ pathways to integrate other inputs to control YO ecdysteroidogenesis.
蜕皮腺(Y 器官或 YO)的转录组包含 48590 个连续序列(重叠群),来自间褪变期(IM)、早期蜕皮前期(EP)、中期蜕皮前期(MP)、晚期蜕皮前期(LP)和蜕皮后期(PM)阶段。在 IM 中,Y 器官通过蜕皮抑制激素(MIH)/环核苷酸依赖性信号保持基础状态。在 EP 中,YO 的激活需要下调 MIH 信号并激活机械靶蛋白(mTOR)依赖性蛋白质合成。在 MP 中,YO 向有丝分裂的转变需要激活素/转化生长因子-β(TGFβ)信号。在 LP 末期,YO 受到抑制。共有 28179 个重叠群(58%)显示出在基因表达上有蜕皮阶段特异性变化。差异表达基因(DEG)数量最多的是 IM/EP(16142 个重叠群)、LP/PM(18161 个重叠群)和 PM/IM(8290 个重叠群)转变。相比之下,EP/MP 和 MP/LP 转变的 DEG 数量分别为 372 和 1502 个重叠群。对 23 个信号转导途径的 DEG 分析显示,MIH、mTOR、激活素/TGFβ、Notch、MAP 激酶和 Wnt 信号显著变化。在蜕皮前期中 MIH 信号基因的下调与 MP 和 LP 中 MIH 敏感性降低一致。IM 和蜕皮前期阶段中 mTOR 信号基因的上调与它在 YO 激活和持续蜕皮甾酮生成中的作用一致。EP 和 MP 中激活素/TGFβ信号基因的上调与肌肉生长抑制素/激活素样因子在 YO 承诺中的作用一致。Notch、MAP 激酶和 Wnt 的 DEG 分析可能表明与 MIH、mTOR 和激活素/TGFβ 途径的可能串扰,以整合其他输入来控制 YO 的蜕皮甾酮生成。