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Tomato Chlorosis Virus Infection Facilitates Bemisia tabaci MED Reproduction by Elevating Vitellogenin Expression

Authors
  • Huang, Liping1, 2
  • Shi, Xiaobin1, 2
  • Shi, Jizhe
  • Zhang, Zhuo2
  • Fang, Yong
  • Zhang, Zhanhong
  • Pan, Qiuyi
  • Zheng, Limin2
  • Gao, Yang2
  • Zhang, Deyong1, 2
  • Tan, Xinqiu2
  • Liu, Yong1, 2
  • Zhou, Xuguo
  • 1 (D.Z.)
  • 2 (X.T.)
Type
Published Article
Journal
Insects
Publisher
MDPI AG
Publication Date
Jan 25, 2021
Volume
12
Issue
2
Identifiers
DOI: 10.3390/insects12020101
PMID: 33503981
PMCID: PMC7911321
Source
PubMed Central
Keywords
Disciplines
  • Article
License
Green

Abstract

Simple Summary The sweet potato whitefly, Bemisia tabaci , is a polyphagous, global invasive insect pest. It can damage vegetables and crops directly by feeding and indirectly by transmitting plant viruses. Previously, we showed that virus infection of host plants can promote B. tabaci MED (Q biotype) reproduction. Here, using a whitefly-tomato chlorosis virus (ToCV)-tomato system, we investigated how ToCV modulates B. tabaci reproduction to facilitate its spread. ToCV infection significantly increased whitefly fecundity and the relative expression of vitellogenin gene ( Vg ). Both ovarian development and fecundity of whitefly were suppressed when Vg expression was silenced with or without ToCV infection. These combined results reveal that ToCV infection increases B. tabaci MED fecundity via elevated vitellogenin gene expression. Abstract Transmission of plant pathogenic viruses mostly relies on insect vectors. Plant virus could enhance its transmission by modulating the vector. Previously, we showed that feeding on virus infected plants can promote the reproduction of the sweet potato whitefly, Bemisia tabaci MED (Q biotype). In this study, using a whitefly-Tomato chlorosis virus (ToCV)-tomato system, we investigated how ToCV modulates B. tabaci MED reproduction to facilitate its spread. Here, we hypothesized that ToCV-infected tomato plants would increase B. tabaci MED fecundity via elevated vitellogenin (Vg) gene expression. As a result, fecundity and the relative expression of B. tabaci MED Vg was measured on ToCV-infected and uninfected tomato plants on days 4, 8, 12, 16, 20 and 24. The role of Vg on B. tabaci MED reproduction was examined in the presence and absence of ToCV using dietary RNAi. ToCV infection significantly increased B. tabaci MED fecundity on days 12, 16 and 20, and elevated Vg expression on days 8, 12 and 16. Both ovarian development and fecundity of B. tabaci MED were suppressed when Vg was silenced with or without ToCV infection. These combined results suggest that ToCV infection increases B. tabaci MED fecundity via elevated Vg expression.

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