RNA sequencing reveals that cell wall, Ca2+, hypersensitive response and salicylic acid signals are involved in pear suspension cells responses to Valsa pyri infection
•Defense-, HR-, Ca2+- cell wall- and hormone-related signals involve in host response.•Functional verification of resistance related genes by Agrobacterium infiltration.•Cell wall remodeling and defense genes MPK4 contributed to Duli-03 tolerance.•SA and Ca2+ related genes obviously weakened the tol...
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Veröffentlicht in: | Scientia horticulturae 2022-11, Vol.305, p.111422, Article 111422 |
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Sprache: | eng |
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Zusammenfassung: | •Defense-, HR-, Ca2+- cell wall- and hormone-related signals involve in host response.•Functional verification of resistance related genes by Agrobacterium infiltration.•Cell wall remodeling and defense genes MPK4 contributed to Duli-03 tolerance.•SA and Ca2+ related genes obviously weakened the tolerance of ‘Yuluxiang’.•HR related signals CDPK also obviously weakened the tolerance of ‘Yuluxiang’.
Pear, one of the staple fruit crops in the world, is under threat from Valsa pyri (Vp) infection. Investigations of the molecular mechanisms underlying pear resistance against Vp infection are largely limited. Using RNA sequencing, we investigated the global gene expression profiles of suspension cells from the resistant rootstock ‘Duli-03′ (Pyrus betulifolia Bunge) and a susceptible cultivar ‘Yuluxiang’ (P. bretschneideri Rehd.) in response to Vp infection. Differentially expressed genes (DEGs) mainly involved in “Cell wall biosynthesis”, “Signal transduction”, “Plant–pathogen interaction”, “Plant hormone signal transduction”, etc., were studied. Further investigations revealed that genes associated with cell wall, Ca2+, hypersensitive response (HR), defense response, and salicylic acid (SA) participated in pear responses to Vp signals. Functional analysis revealed that defense-related genes PbeKCS1/10-1 and PbeMPK4-1 positively regulated Vp resistance in pear fruit, whereas four TGACG motif binding factor (TGA) genes played a negative regulatory role. |
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ISSN: | 0304-4238 1879-1018 |
DOI: | 10.1016/j.scienta.2022.111422 |