No abstract

An outbreak of a new disease occurred in cotton (Gossypium hirsutum) fields in northwest Argentina starting in the 2009-10 growing season and is still spreading steadily. The characteristic symptoms of the disease included slight leaf rolling and a bushy phenotype in the upper part of the plant. In this study, we determined the complete nucleotide sequences of two independent virus genomes isolated from cotton blue disease (CBD)-resistant and -susceptible cotton varieties. This virus genome comprised 5,866 nucleotides with an organization similar to that of the genus Polerovirus and was closely related to cotton leafroll dwarf virus, with protein identity ranging from 88 to 98%. The virus was subsequently transmitted to a CBD-resistant cotton variety using Aphis gossypii and symptoms were successfully reproduced. To study the persistence of the virus, we analyzed symptomatic plants from CBD-resistant varieties from different cotton-growing fields between 2013 and 2015 and showed the presence of the same virus strain. In addition, a constructed full-length infectious cDNA clone from the virus caused disease symptoms in systemic leaves of CBD-resistant cotton plants. Altogether, the new leafroll disease in CBD-resistant cotton plants is caused by an atypical cotton leafroll dwarf virus.

Cotton blue disease (CBD) is the most important disease present in cotton crops in South America and cotton leafroll dwarf virus (CLRDV) is the causal agent. The disease has been controlled by sowing cotton varieties resistant to CLRDV. However, in the 2009/10 growing season, an outbreak due to an atypical CLRDV isolate (CLRDV‐at) occurred in northwest Argentina. Although CLRDV and CLRDV‐at genomes are very closely related, the symptoms they produce in cotton plants are quite different. P0 is the most divergent protein between the isolates and in CLRDV is a silencing suppressor protein. This work characterized the silencing suppressor activity of the P0 protein encoded by CLRDV‐at (P0CL‐at) and evaluated its role in Cbd‐resistance break in cotton plants. It was demonstrated that P0CL‐at, despite having a mutation in the consensus of the F‐box‐like motif, was able to suppress local RNA silencing, but displayed lower activity than P0CL. P0CL and P0CL‐at showed no differences in the interaction with Gossypium hirsutum SKP1 orthologue (GSK1) and Nicotiana benthamiana SKP1 and both P0 proteins triggered destabilization of ARGONAUTE1. However, when the ability to enhance PVX symptoms was evaluated, P0CL‐at was shown to be a weaker pathogenicity factor than P0CL in N. benthamiana. Interestingly, trans‐expressed P0CL‐at enabled CLRDV to systemically infect CBD‐resistant plants, and a chimeric CLRDV‐P0CL‐at infectious clone succeeded in establishing infection in CBD‐resistant cotton varieties with symptoms resembling those produced by CLRDV‐at. These results strongly suggest that P0CL‐at is the avirulence (Avr) determinant involved in breaking cotton Cbd gene‐based resistance.