Transcriptome Analysis of a Cotton Cultivar Provides Insights into the Differentially Expressed Genes Underlying Heightened Resistance to the Devastating Verticillium Wilt
Cotton is an important economic crop worldwide. Verticillium wilt (VW) caused by ( ) is a serious disease in cotton, resulting in massive yield losses and decline of fiber quality. Breeding resistant cotton cultivars is an efficient but elaborate method to improve the resistance of cotton against in...
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Published in | Cells (Basel, Switzerland) Vol. 10; no. 11; p. 2961 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
30.10.2021
MDPI |
Subjects | |
Online Access | Get full text |
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Summary: | Cotton is an important economic crop worldwide. Verticillium wilt (VW) caused by
(
) is a serious disease in cotton, resulting in massive yield losses and decline of fiber quality. Breeding resistant cotton cultivars is an efficient but elaborate method to improve the resistance of cotton against
infection. However, the functional mechanism of several excellent VW resistant cotton cultivars is poorly understood at present. In our current study, we carried out RNA-seq to discover the differentially expressed genes (DEGs) in the roots of susceptible cotton
cultivar Junmian 1 (J1) and resistant cotton
cultivar Liaomian 38 (L38) upon
991 inoculation at two time points compared with the mock inoculated control plants. The potential function of DEGs uniquely expressed in J1 and L38 was also analyzed by GO enrichment and KEGG pathway associations. Most DEGs were assigned to resistance-related functions. In addition, resistance gene analogues (RGAs) were identified and analyzed for their role in the heightened resistance of the L38 cultivar against the devastating
991. In summary, we analyzed the regulatory network of genes in the resistant cotton cultivar L38 during
infection, providing a novel and comprehensive insight into VW resistance in cotton. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 2073-4409 2073-4409 |
DOI: | 10.3390/cells10112961 |