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Histological Mechanisms of the Resistance Conferred by the Ma Gene Against Meloidogyne incognita in Prunus spp.

First, second, third, fourth, and sixth authors: INRA, UMR Interactions Biotiques et Santé Végétale, UMR INRA 1301, CNRS 6243, and Université de Nice Sophia-Antipolis, F-06903 Sophia-Antipolis, France; and fifth author: Ecole Nationale d'Agriculture, Département de Protection des Plantes, 50000 Meknès, Morocco.

The Ma gene from Myrobalan plum is a TNL gene that confers a high-level resistance to all root-knot nematodes of major economic importance, including Meloidogyne incognita, M. javanica, M. arenaria, and M. enterolobii. The nematode behavior in the roots and the corresponding histological mechanisms of the Ma resistance to M. incognita in the resistant (R) accessions of the plum ‘P.2175’ and the interspecific hybrid P.2175 × almond-peach ‘35’, carrying the Ma1 allele (Ma1/ma), were characterized in comparison with the susceptible (S) accessions in the plum ‘P.2032’ and the interspecific hybrid P.2175 × almond-peach ‘253’ (ma/ma). Second-stage juveniles (J2s) were inoculated in micropropagated plantlets grown in soil substrate under controlled conditions at 25°C. Nematodes penetrated both R and S plants preferentially along the apical zone or close to the young lateral buds and moved via similar routes. Then they migrated into the cortex downward in the direction of the apex and turned up in the meristematic apical region to colonize the differentiating stele. In R accessions, motile J2s neither swelled nor developed into J3s, and initiation of feeding sites was never observed. This complete absence of gall symptoms is associated with cell necroses and corresponding hypersensitive-like reaction (HLR) phenotypes occurring either in the stele or in the meristematic apical region or in the cortex. Nematode attacks often disorganized the meristematic apical tissues of R accessions, which induced the development of subterminal lateral roots replacing primary terminal apices and, thus, provided an active resistance reaction to HLR damage.