No abstract

Many factors contribute to a decline in production of cocoa beans worldwide. Plant diseases such as black pod, witches' broom, and frosty pod rot are major components of the decline in production. Plant pathologists and microbiologists must discover and devise means to reduce disease losses and to save chocolate for the enthusiastic consumers of the world. This review discusses the major disease of cacao and their effect on world production. Accepted for publication 14 June 2001. Published 9 July 2001.

Verticillium wilt (VW), caused by the soil‐borne fungus Verticillium dahliae Kleb., is one of the most destructive diseases in Upland cotton (Gossypium hirsutum L.) production in the U.S. and worldwide. Development of VW‐resistant cultivars remains the only economic option for controlling the disease. The objective of this review was to summarize the progress in screening methods, resistance sources, and genetics, quantitative trait locus (QTL) mapping, marker‐assisted selection (MAS) and breeding for VW resistance in cotton. Even though Gossypium barbadense L. carries high levels of resistance, its resistance has not been transferred into commercial Upland cultivars. Many Acala cotton cultivars developed in New Mexico and California between the 1940s and the 1990s, and some commercial transgenic cultivars are tolerant or moderately resistant to VW. However, due to difficulties in achieving consistent and uniform inoculation and infection with V. dahliae, both qualitative and quantitative inheritance of VW resistance have been reported in numerous studies for resistant G. barbadense and Upland genotypes. Several QTL analyses have shown the existence of VW resistance QTLs on almost all the tetraploid cotton chromosomes; however, QTLs have most frequently been detected on c5, c7, c8, c11, c16, c17, c19, c21, c23, c24, and c26. This has led to MAS for progeny with favorable QTL alleles for VW resistance in several experiments. Phenotypic selection for VW resistance has been inefficient, while the effectiveness and efficiency of MAS remain to be validated. There is an urgent need for the development of better plant inoculation and screening methods, and for more molecular mapping studies to discern the genetic basis of VW resistance in cotton.

BackgroundVerticillium wilt (VW) and Fusarium wilt (FW), caused by the soil-borne fungi Verticillium dahliae and Fusarium oxysporum f. sp. vasinfectum, respectively, are two most destructive diseases in cotton production worldwide. Root-knot nematodes (Meloidogyne incognita, RKN) and reniform nematodes (Rotylenchulus reniformis, RN) cause the highest yield loss in the U.S. Planting disease resistant cultivars is the most cost effective control method. Numerous studies have reported mapping of quantitative trait loci (QTLs) for disease resistance in cotton; however, very few reliable QTLs were identified for use in genomic research and breeding.ResultsThis study first performed a 4-year replicated test of a backcross inbred line (BIL) population for VW resistance, and 10 resistance QTLs were mapped based on a 2895 cM linkage map with 392 SSR markers. The 10 VW QTLs were then placed to a consensus linkage map with other 182 VW QTLs, 75 RKN QTLs, 27 FW QTLs, and 7 RN QTLs reported from 32 publications. A meta-analysis of QTLs identified 28 QTL clusters including 13, 8 and 3 QTL hotspots for resistance to VW, RKN and FW, respectively. The number of QTLs and QTL clusters on chromosomes especially in the A-subgenome was significantly correlated with the number of nucleotide-binding site (NBS) genes, and the distribution of QTLs between homeologous A- and D- subgenome chromosomes was also significantly correlated.ConclusionsTen VW resistance QTL identified in a 4-year replicated study have added useful information to the understanding of the genetic basis of VW resistance in cotton. Twenty-eight disease resistance QTL clusters and 24 hotspots identified from a total of 306 QTLs and linked SSR markers provide important information for marker-assisted selection and high resolution mapping of resistance QTLs and genes. The non-overlapping of most resistance QTL hotspots for different diseases indicates that their resistances are controlled by different genes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1682-2) contains supplementary material, which is available to authorized users.

No abstract

No abstract

Fusarium wilt (FW), caused by the soilborne fungus Fusarium oxysporum f. sp. vasinfectum (FOV), with eight races recognized, is one of the most destructive diseases in cotton (Gossypium spp.). Employment of FW‐resistant cultivars has proven to be the most cost‐effective method to control the disease. This review provides a comprehensive synthesis of research progress in breeding, genetics, and molecular mapping of FW resistance. A focused pedigree analysis in Upland cotton (G. hirsutum L.) has identified five major FW‐resistant sources (‘Dillon’, ‘Dixie Triumph’, ‘Cook 307‐6’, ‘Coker Clevewilt’, and ‘Wild’) in the United States and three (‘Chuan 52‐128’, ‘Chuan 57‐681’, and ‘CRI 12’) in China. The use of numerous early segregating populations has consistently confirmed the predominant presence of additive gene effects on FW resistance; however, heritability is usually low because of high experimental error. Several mapping studies have detected approximately 40 quantitative trait loci (QTL) on 19 chromosomes. A number of qualitative genetic studies have identified five major resistance genes in Upland and Pima (G. barbadense L.) cotton including Fw1, Fw2, FwR (chromosome 17), FOV1 (chromosome 16), and FOV4 (chromosome 14). There are other major resistance genes identified through marker or segregating analysis, but methods with high and uniform infection by FOV are required to confirm the results. More differential hosts should be developed to differentiate new races, and more resistance genes from new sources should be identified for their strategic deployment in preventing a possible risk of disease epidemic.

No abstract