# Sec61s and Sec62/Sec63 Genes Are Essential for Survival by Regulating the Gut and Cuticle Development in Locusta migratoria

## TL;DR

This study shows that certain genes are crucial for gut and cuticle development in locusts, making them potential targets for locust control.

## Contribution

The study identifies and functionally characterizes Sec61 and Sec62/Sec63 genes in Locusta migratoria for the first time.

## Key findings

- Silencing LmSec61α and LmSec61γ causes gut defects and 100% mortality in locusts.
- Knockdown of LmSec62 and LmSec63 disrupts molting and cuticle formation.
- These genes are highly expressed in multiple tissues, including the integument.

## Abstract

Sec61 channel and Sec62/Sec63 complex play key roles in the protein translocation. In this study, Sec61α, Sec61β, Sec61γ, Sec62 and Sec63 were identified in Locusta migratoria. Then, the functions of these genes were explored using RNA interference. Silencing LmSec61α and LmSec61γ lead to the feeding cessation, with the defective structure of the midguts and gastric caecum. But the simultaneous RNAi of LmSec62 and LmSec63 disrupted locusts molting by regulating the cuticle formation in the nymphal stages.

In eukaryotes, a lot of proteins are transported across the endoplasmic reticulum by the heterotrimeric Sec61 channel. And post-translational transport needs another Sec62/Sec63 complex. However, functions of these genes are poorly explored in insects. In this study, we first identified five Sec genes, named Sec61α, Sec61β, Sec61γ, Sec62 and Sec63, in Locusta migratoria. Quantitative reverse-transcription polymerase chain reaction (RT-qPCR) analysis showed that these five genes were expressed in muti-tissues, including wing pad, leg, foregut, midgut, gastric cecum, hindgut, and highly expressed in the integument. Knockdown of LmSec61α and LmSec61γ by RNA interference (RNAi) lead to the feeding cessation with a mortality rate of 100%. However, there is only 13.4% of dsLmSec61β-injected nymphs died before molting. All nymphs injected with dsLmSec61α and dsLmSec61γ died before molting with the gut atrophy. Furthermore, hematoxylin–eosin staining indicated that the cells of the midguts and gastric caecum were defective, and the microvilli and peritrophic matrix were destroyed seriously after silencing LmSec61α and LmSec61γ. Knockdown of LmSec62 and LmSec63 resulted in high mortality before and during molting. The hematoxylin–eosin (HE) staining and transmission electron microscopy (TEM) results showed that both the formation of the new cuticle and the degradation of the old cuticle were inhibited in dsLmSec63-injected insects compared to the controls. Especially, there was no obvious plaques on microvillar tips of the epidermal cells after silencing of LmSec63. These results revealed that Sec61s and Sec62/Sec63 genes are required in the gut and cuticle development of locusts. Therefore, these genes are potential targets for the control of locusts.