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Volume 60 - Tomato Genetics Cooperative - University of Florida

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esistance, and breeding in geographical areas where different strains <strong>of</strong> bacterial wilt<br />

are prevalent, the breeders exploited the genetic potentialities at their disposal, and<br />

created material resisting a wide range <strong>of</strong> bacterial wilt strains as exemplified by the<br />

results obtained in the worldwide trial carried out by Wang et al. (1998). Indeed, the top<br />

nine resistant accessions which had high levels <strong>of</strong> resistance in almost all 12 locations<br />

tested (>90% survival on average) were developed in Hawaii („H7996‟, „H7997 S and<br />

L‟, „H7998 S and M‟), Philippines („TML46‟ and „TML114‟, „R3034‟), and Japan („BF-<br />

Okitsu‟).<br />

Other sources <strong>of</strong> resistance in wild tomatoes have been described sporadically in<br />

the literature in accessions <strong>of</strong> the same species (S. pimpinellifolium, cherry and pear S.<br />

lycopersicum) as well as in other wild relatives <strong>of</strong> tomato (Laterrot & Kaan, 1977;<br />

Jaworski et al., 1987; Anaïs, 1997; Mohamed et al., 1997; Carmeille et al. 2006b; Hai et<br />

al., 2008). From these results, it seems that resistance to bacterial wilt is not that<br />

frequent in tomato germplasm. The high genetic diversity displayed by Ralstonia<br />

solanacearum complex (Fegan & Prior, 2005) and the strong interactions between<br />

strains and resistant material (Lebeau et al., 2011) suggest that various resistance<br />

mechanisms, including strain specific ones, exist in tomato resistant germplasm.<br />

Therefore, breeders have some opportunities at their disposal to enlarge the relatively<br />

narrow range <strong>of</strong> resistance sources primarily used so far, and to continue accumulating<br />

different mechanisms <strong>of</strong> resistance in tomato genotypes to obtain better stability <strong>of</strong><br />

resistance in different environments. However, they might be limited by the fact that<br />

some bacterial strains are not controlled by any resistant accession (see section 5.<br />

below).<br />

Inheritance studies have focused mostly on F2, F3 and RILs progenies <strong>of</strong> „Hawaii<br />

7996‟ crossed with the susceptible „WVa700‟ (S. pimpinellifolium). Several QTLs <strong>of</strong><br />

resistance have been identified, including a major QTL on chromosome 6 effective<br />

towards „GMI8217‟, an isolate <strong>of</strong> race 1 biovar 1 (Thoquet et al. 1996a & b); <strong>of</strong> „Pss4‟,<br />

an isolate <strong>of</strong> race 1, biovar 3, phylotype 1 (Wang et al., 1998); and „JT516‟, an isolate<br />

representative <strong>of</strong> race 3-phylotype II (Carmeille et al., 2006a). Wang et al. (2000)<br />

identified another major QTL <strong>of</strong> resistance <strong>of</strong> „Hawaii 7996‟ effective towards „Pss4‟ and<br />

located on chromosome 12. Several minor QTLs located on chromosomes 3, 4, 8,<br />

some <strong>of</strong> which having a season dependent expression (Carmeille et al., 2006a) have<br />

also been identified. Mejia et al (2009) confirmed the QTLs on chromosome 6 and 12<br />

were associated with resistance in „Hawaii 7996‟ observed in Guatemala field evaluation<br />

against local phylotype I strains. Work is ongoing at AVRDC for adding markers to the<br />

QTLs regions <strong>of</strong> „Hawaii 7996‟ associated to resistance to bacterial strains belonging to<br />

phylotype I, in order to develop tools for marker assisted selection.<br />

QTLs <strong>of</strong> resistance <strong>of</strong> the resistant line „L285‟ effective towards „UW364‟ an isolate<br />

<strong>of</strong> race 1, biovar 4, have also been located on chromosomes 6, as well as on<br />

chromosomes 7 and 10 (Danesh et al., 1994). Pattern <strong>of</strong> resistance derived from<br />

CRA66 has been described as polygenic (Prior et al., 1994) but no molecular data are<br />

available for this source.<br />

15

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