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ARS Home » Southeast Area » Gainesville, Florida » Center for Medical, Agricultural and Veterinary Entomology » Chemistry Research » Research » Publications at this Location » Publication #310274
Title: Mi-1-mediated nematode resistance in tomatoes is broken by short-term heat stress but recovers over time

Author
item MARQUES DE CARVALHO, LUCIANA - Embrapa
item Benda, Nicole
item Vaughan, Martha
item Cabrera Cordon, Ana
item Hung, Kaddie
item Cox, Thomas
item Abdo, Zaid
item ALLEN, L.HARTWELL - Retired ARS Employee
item Teal, Peter

Submitted to: Journal of Nematology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/6/2015
Publication Date: 7/8/2015
Citation: Marques De Carvalho, L., Benda, N.D., Vaughan, M.M., Cabrera Cordon, A.R., Hung, K., Cox, T.R., Abdo, Z., Allen, L., Teal, P.E. 2015. Mi-1-mediated nematode resistance in tomatoes is broken by short-term heat stress but recovers over time. Journal of Nematology. 47(2):133-140.

Interpretive Summary: Root-knot nematode (RKN) infection results in significant economic losses of tomato worldwide. The only available source of resistance to RKN in tomato is a single, dominant gene named Mi-1, which if present in the genome typically confers resistance resulting in less root gall formation. Heat stress however, appears to interfere with the effect of this resistance leading to inconsistent results and outbreaks of increased crop losses. Through an analysis of midday heat exposure, scientists at the USDA-ARS Center for Medical, Agricultural and Veterinary Entomology in Gainesville, Florida, discovered that a single 3 h midday heat treatment of 35ºC was sufficient to break Mi-1 gene resistance in tomato cultivar Amelia. This heat-associated breakdown of Mi-1-conferred resistance recovers however with time. Additional heat treatments and/ or nematode infection does not further increase the susceptibility of the plants nor does it inhibit the timing of recovery. Changes in susceptibility do not appear to be regulated at the transcriptional level, as Mi-1 gene relative transcripts were unaltered by both heat treatment and RKN infection. These findings which have more accurately characterized the timing of heat-associated breakdown of Mi-1-conferred resistance should aid in the development of strategies to protect the crop at this time of heightened susceptibility.

Technical Abstract: In tomato (Solanum lycopersicum Mill.), the only available genomic resource of resistance to root-knot nematodes (RKN; Meloidogyne incognita, M. javanica and M. arenaria), which are considered among the most devastating crop pests worldwide, is a single dominant gene termed Mi-1. Heat stress is thought to break Mi-1-associated resistance, but inconsistent results in published field and greenhouse literature led us to test the effect of short-term midday heat stress on the susceptibility of tomato to RKN. Initially, we verified the genomic presence or absence of the Mi-1 gene in two S. lycopersicum cvs. Amelia and Rutgers, and tested for resistance to M. incognita infection. At controlled day/night temperatures of 25°C/ 21°C, Amelia was deemed resistant (4.1 ± 0.4 galls/ plant) and Rutgers susceptible (132 ± 9.9 galls/ plant) to M. incognita infection. However, exposure to a single 3h heat spike of 35ºC increased the susceptibility of Amelia, leading to the production of 3.4-fold more galls, in comparison to control plants at 25°C. However, the heat-induced breakdown of Mi-1 resistance in Amelia recovered with time. Additional days of the heat treatment did not increase susceptibility or hinder resistance recovery. Furthermore, a second inoculation of previously heat-treated and RKN-infected Amelia did not result in further gall formation, suggesting that previous nematode infection also does not increase susceptibility or hinder resistance recovery. Thus our findings show a single 3 h midday heat treatment of 35ºC is sufficient to break Mi-1 gene resistance in tomato cultivar Amelia, however resistance recovers with time regardless of additional heat exposures and RKN infection. Furthermore, changes in Mi-1 gene resistance do not appear to be regulated at the transcriptional level, since Mi-1 gene transcription was unaltered by heat treatment and RKN infection. These findings which have more accurately characterized the timing of heat-associated breakdown of Mi-1-conferred resistance should aid in the development of strategies to protect the tomatoes at times of heightened susceptibility.