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Deficiency of ULK1/ATG1 in the follicle cells disturbs ER homeostasis and causes defective chorion deposition in the vector Rhodnius prolixus
Author(s) -
Bomfim Larissa,
Ramos Isabela
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202001396r
Subject(s) - rhodnius prolixus , microbiology and biotechnology , biology , gene silencing , oogenesis , unfolded protein response , autophagy , rna interference , endoplasmic reticulum , oocyte , rna , genetics , ecology , embryo , apoptosis , insect , gene
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.