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Genetic analysis of resistance to Phoma tracheiphila in three Citrus and Poncirus progenies
Author(s) -
Recupero G. Reforgiato,
Gentile A.,
Russo M. P.,
Domina F.
Publication year - 1997
Publication title -
plant breeding
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.583
H-Index - 71
eISSN - 1439-0523
pISSN - 0179-9541
DOI - 10.1111/j.1439-0523.1997.tb02180.x
Subject(s) - biology , allele , genetics , major gene , plant disease resistance , gene , genotype , botany
Mal secco is a serious tracheomycosis, caused by the fungus Phoma tracheiphila (Petri) Kanc, et Ghik., which attacks some species of the genus Citrus . The considerable amount of time and space required to evaluate host plant response has discouraged research on the mechanism of inheritance involved in the susceptibility to this disease. The aim of the present work was to study segregation of the resistance trait in three progenies obtained by crossing Citrus latipes (Swing.) Tan., as a female parent, with the male parents Poncirus trifoliata (L.) Raf., C.aurantium L. and C. volkameriana Pasq. Resistance determination was based on natural infections observed over 10 years. Results allowed us to hypothesize three alternative genes (A, B and C) which determine dominant resistance as opposed to susceptibility: the presence of a single allele can thus confer resistance. In addition, we suggest the existence of a fourth gene which, in conditions of dominance, is able to determine susceptibility by nullifying the action of the dominant B allele. Response to the pathogen was also associated with the production of chitinase a PR (pathogenesis‐related) protein reported to be present in great quantities in mal secco‐resistant Citrus genotypes. Segregation analysis of one F 2 progeny confirmed the hypothesis that the resistance trait is controlled by at least two dominant genes. Further evidence is needed to ascertain whether this hypothesis is applicable to other Citrus species, in which the possibility of other genetic mechanisms being implicated cannot be ruled out, thus making the genetic basis of mal secco resisance more complex.