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Phenotypic Expression, Stability, and Inheritance of a Recessive Resistance to Monopartite Begomoviruses Associated with Tomato Yellow Leaf Curl Disease in Tomato

First and sixth authors: Laboratorio de Virología Vegetal, Est. Exp. La Mayora, Consejo Superior de Investigaciones Científicas (CSIC), E-29750 Algarrobo-Costa, Málaga, Spain; second author: Departamento de Biologia Celular, Universidade de Brasília (UnB), 70910-970 Brasília-DF, Brazil; third and fourth authors: Embrapa Vegetable Crops, National Center for Vegetable Crops Research (CNPH), CP 218, 70359-970 Brasília-DF, Brazil; and fifth author: Departamento de Mejora Vegetal, Est. Exp. La Mayora, CSIC, E-29750 Algarrobo-Costa, Málaga, Spain.

Tomato-infecting begomoviruses comprise a complex of monopartite and bipartite virus species that cause severe yield and quality losses worldwide. Therefore, the availability of wide spectrum resistance for begomovirus control is desirable. However, limited sources of resistance are available. In this study, three tomato inbred lines with resistance to bipartite begomoviruses of Brazil were tested for resistance to monopartite begomoviruses associated with the tomato yellow leaf curl disease (TYLCD). Stable resistance to Tomato yellow leaf curl virus was observed either by inoculation with Bemisia tabaci or with Agrobacterium tumefaciens using an infectious clone. The resistance resulted in a complete absence of TYLCD symptoms and restricted virus accumulation. Further studies performed with the line ‘468-1-1-12’ indicated that the resistance was also effective against three other virus species associated with TYLCD, indicating wide spectrum resistance of this source. Quantitative genetics analyses suggested that a major recessive locus with epistatic interactions is controlling the resistance to TYLCD in ‘468-1-1-12’, which could facilitate introgression of this trait into elite tomato lines. The resistance was stable under field conditions with high TYLCD pressure. Mild symptoms could be observed in these conditions, and recovery from disease and from virus infection suggested an active host antiviral defense mechanism. The differential reaction of ‘468-1-1-12’ against a number of TYLCD-associated viruses and artificial chimeras between them allowed to identify a region of the virus genome that presumably contains a virus determinant for breaking the resistance to infection observed in ‘468-1-1-12’.