Heidi Lynn Stevens-Robbins and Dr. Eric N. Jellan, Agronomy & Horticulture
Tomato yellow leaf curl virus (TYLCV) and tomato mottle virus (ToMoV), are both geminiviruses, and are considered major limiting factors in the commercially grown tomato (Lycopersicon esculentum Mill.) in Florida and the Middle East (1). These viruses have been identified as reducing yields and/or reducing fruit quality in an infected crop. TYLCV appears to have originated in Old World and has been recently identified in Florida (1). ToMoV was originally identified in Florida and has since been found throughout the Southeastern United States (2).
Both of these diseases are vectored by the whitefly Bemisia argentifolii Perring et al. (3). This whitefly, at present, is controlled with the use of pesticides, which in turn reduces but does not eliminate the incidence of these diseases. However, natural virus resistance would allow reduced usage of pesticides and higher levels of marketable fruit. High levels of resistance to both TYLCV and ToMoV has been identified in the wild tomato species “L. chilense” Dun. A ToMoV resistance-breeding program utilizing L. chilense was initiated in Florida in 1990 (4). Results are interesting when compared to a study identified a TYLCV-resistance gene, TY-1, which was also derived from L. chilense. This gene was located on chromosome 6 in the tomato genome (5). However, several studies show that TY-1, alone does not provide resistance to ToMoV.
Several preliminary studies in Florida show a strong indication that ToMoV resistance is multigenic. It was our hypothesis that one or more genes responsible for resistance to ToMoV reside on chromosome 6. It is probable that additional genes responsible for resistance to this disease resides elsewhere in the genome.
In order to obtain more data on the possible significance of the genetics of chromosome 6 for resistance to ToMoV derived from L. chilense, I proposed to use ten RFLP (restriction fragment length polymorphisms) probes distributed equally along the length of chromosome 6. These probes would allow me to identify if those ten areas in the genome originated from L. chilense or from the cultivated tomato.
Initially, we planned to test these markers on approximately 60 highly resistant tomato plants selected from a ToMoV resistance segregating population of over 300 F2 plants. This test would have allowed us to determine areas on chromosome 6 associated with ToMoV resistance.
Originally, we encounter the problem of insufficient DNA. The samples collected from Florida were the only samples available. As a result it was decided to use ten highly resistant lines which are genetically uniform within each line, but genetically different between lines. These plants were grown and sufficient DNA was collected.
After several RFLP markers were tested results indicated that some regions, near the telomere (tip of the chromosome) on the shorter arm, are L. chilense derived. Which means that, these L. chilense areas may be required for ToMoV resistance. This logic comes from the concept that all ten lines contained the same regions of L. chilense derived DNA, and resistance is known to be from L. chilense. This work is being continued on a more detailed scale down the entire chromosome.
In conclusion, the results of these data have helped in determining our hypothesis that genes responsible for ToMoV resistance are found on chromosome 6. Finally, this study should be considered as a preliminary study for looking at the remaining 11 chromosomes of the tomato genome.
References:
- Czonsnek H et al. (1990) Phytophath Medit 29:1-6.
- Polston JE et al. (1995) Plant Dis. 79:539.
- Rochester DE et al. (1994) J Gen Virol 75:477-485
- Scott JW et al. (1996) In: Bemisia 1995: Taxonomy, Biology, Damage Control and Management 30:357-367
- Zamir D et al. (1994) Theo Appl Genet 88:141-146