Sheath blight (ShB) disease, caused by
Rhizoctonia solani, is an economically important rice
disease worldwide, especially in intensive production
systems. Several studies have been conducted to
identify sources for ShB resistance in different
species of rice, including local accessions and
landraces. To date, none of the genotypes screened
are immune to ShB, although variation in levels of
resistance have been reported. Several quantitative
trait loci (QTL) for ShB resistance have been
identified using mapping populations derived from
indica or japonica rice. A total of 33 QTL associated
with ShB resistance located on all 12 rice chromosomes
have been reported, with ten of these colocalizing
with QTL for morphological attributes,
especially plant height, or for heading date. Sixteen
QTL, from the same or differing genetic backgrounds,
have been mapped at least twice. Of these,
nine QTL were independent of morphological traits
and heading date. We hypothesize that two main,
distinct, mechanisms contribute to ShB resistance:
physiological resistance and disease escape. Strategies
to improve our understanding of the genetics of
resistance to ShB are discussed.
Sheath blight (ShB) disease, caused byRhizoctonia solani, is an economically important ricedisease worldwide, especially in intensive productionsystems. Several studies have been conducted toidentify sources for ShB resistance in differentspecies of rice, including local accessions andlandraces. To date, none of the genotypes screenedare immune to ShB, although variation in levels ofresistance have been reported. Several quantitativetrait loci (QTL) for ShB resistance have beenidentified using mapping populations derived fromindica or japonica rice. A total of 33 QTL associatedwith ShB resistance located on all 12 rice chromosomeshave been reported, with ten of these colocalizingwith QTL for morphological attributes,especially plant height, or for heading date. SixteenQTL, from the same or differing genetic backgrounds,have been mapped at least twice. Of these,nine QTL were independent of morphological traitsand heading date. We hypothesize that two main,distinct, mechanisms contribute to ShB resistance:physiological resistance and disease escape. Strategiesto improve our understanding of the genetics ofresistance to ShB are discussed.
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