Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
INCT-EM/CNPq, Rio de Janeiro, Brazil.
FASEB J. 2020 Oct;34(10):13561-13572. doi: 10.1096/fj.202001396R. Epub 2020 Aug 26.
In insects, synthesis and deposition of the chorion (eggshell) are performed by the professional secretory follicle cells (FCs) that surround the oocytes in the course of oogenesis. Here, we found that ULK1/ATG1, an autophagy-related protein, is highly expressed in the FCs of the Chagas-Disease vector Rhodnius prolixus, and that parental RNAi silencing of ULK1/ATG1 results in oocytes with abnormal chorion ultrastructure and FCs presenting expanded rough ER membranes as well as increased expression of the ER chaperone BiP3, both indicatives of ER stress. Silencing of LC3/ATG8, another essential autophagy protein, did not replicate the ULK1/ATG1 phenotypes, whereas silencing of SEC16A, a known partner of the noncanonical ULK1/ATG1 function in the ER exit sites phenocopied the silencing of ULK1/ATG1. Our findings point to a cooperated function of ULK1/ATG1 and SEC16A in the FCs to complete choriogenesis and provide additional in vivo phenotype-based evidence to the literature of the role of ULK1/ATG1 in the ER in a professional secretory cell.
在昆虫中，卵壳（蛋壳）的合成和沉积是由围绕卵母细胞在卵发生过程中的专业分泌滤泡细胞（FCs）完成的。在这里，我们发现自噬相关蛋白 ULK1/ATG1 在恰加斯病传播媒介丽蝇的 FCs 中高度表达，并且 ULK1/ATG1 的亲本 RNAi 沉默导致卵母细胞具有异常的卵壳超微结构，并且 FCs 呈现扩张的粗面内质网膜以及内质网伴侣 BiP3 的表达增加，这两者都表明内质网应激。另一种必需的自噬蛋白 LC3/ATG8 的沉默并没有复制 ULK1/ATG1 的表型，而 SEC16A 的沉默，一种已知的非典型 ULK1/ATG1 在 ER 出口位点的功能的伴侣，复制了 ULK1/ATG1 的沉默。我们的发现表明 ULK1/ATG1 和 SEC16A 在 FCs 中具有协同功能，以完成卵壳发生，并为 ULK1/ATG1 在专业分泌细胞中在 ER 中的作用的文献提供了额外的基于表型的体内证据。
