Transferring cercospora leaf sopt resistance from Beta maritima to sugarbeet by backcrossing

Bilgen, Talat; Gaskill, J. O.; Hecker, R. J.; Wood, D. R.

doi:10.5274/jsbr.15.5.444

Cited by 15 publications

(8 citation statements)

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“…In earlier CLS-resistant germplasm from Fort Collins, an estimated 4 or 5 genes are responsible for CLS resistance (Smith and Gaskill 1970), and broad-sense heritability estimates ranged from 12 to 71% (Bilgen et al 1969), with narrow-sense heritability estimates of about 24%. An estimate of 44-62% of the variation was due environment in this test (Smith and Ruppel 1974).…”

Section: Resources Expendedmentioning

confidence: 99%

Broadening the genetic base of sugar beet: introgression from wild relatives

2006

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The development of sugar beet as an economically important field crop coincided with our increased understanding of modern genetic principles. It was developed in the late 1700s from white fodder beet; therefore, the genetic base of sugar beet is thought to be narrower than many open-pollinated crops. The wild sea beet is the progenitor of all domesticated beet and cross compatible with cultivated beet (domestic and cultivated are given subspecies level in the same species). The breeding system of sugar beet is complex and the crop is biennial, which lengthens the generation time to almost 1 year. A geneticcytoplasmic male sterility (CMS) system is utilized for commercial hybrid production. Early breeding objectives were to improve the concentration and extractability of sucrose and little emphasis was placed on host-plant resistance to insect, nematode, and disease pests. As production areas expanded, these pests limited production, sometimes severely. The first systematic L. Panella (

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Section: Resources Expendedmentioning

confidence: 99%

Broadening the genetic base of sugar beet: introgression from wild relatives

2006

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“…Different germplasm, population structures, environments, set‐ups of the experiments and formula have been applied to this analysis. Some studies revealed higher heritability estimates ranging from > 0.8 (Schäfer‐Pregl et al ., 1999; one F 2 and one related top‐cross population, two environments, calculated with repeated measurements), and 0.80 (Koch and Jung, 2000; one F 2 population, microenvironments used for calculation) to 0.60–0.71 (Smith and Gaskill, 1970; three populations, 2 years, 40 replications each), whereas for others lower heritabilities from 0.24 (Smith and Ruppel, 1974; two populations), 0.17– > 0.8 (Saito, 1966; various populations, years, methods) to 0.12–0.16 (Bilgen et al ., 1969; two open‐pollinated back‐cross populations) were reported. These studies underline the difficulties in studying inheritance of resistance to Cercospora beticola , although all report that resistance is based mostly on additive components.…”

Section: Resistance Genes and Mechanismsmentioning

confidence: 99%

Sugarbeet leaf spot disease (Cercospora beticola Sacc.)†

Weiland

Koch²

2004

Molecular Plant Pathology

153

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SUMMARY Leaf spot disease caused by Cercospora beticola Sacc. is the most destructive foliar pathogen of sugarbeet worldwide. In addition to reducing yield and quality of sugarbeet, the control of leaf spot disease by extensive fungicide application incurs added costs to producers and repeatedly has selected for fungicide‐tolerant C. beticola strains. The genetics and biochemistry of virulence have been examined less for C. beticola as compared with the related fungi C. nicotianae, C. kikuchii and C. zeae‐maydis, fungi to which the physiology of C. beticola is often compared. C. beticola populations generally are not characterized as having race structure, although a case of race‐specific resistance in sugarbeet to C. beticola has been reported. Resistance currently implemented in the field is quantitatively inherited and exhibits low to medium heritability. Taxonomy: Cercospora beticola Sacc.; Kingdom Fungi, Subdivision Deuteromycetes, Class Hyphomycetes, Order Hyphales, Genus Cercospora. Identification: Circular, brown to red delimited spots with ashen‐grey centre, 0.5–6 mm diameter; dark brown to black stromata against grey background; pale brown unbranched sparingly septate conidiophores, hyaline acicular conidia, multiseptate, from 2.5 to 4 µm wide and 50–200 µm long. Host range: Propagative on Beta vulgaris and most species of Beta. Reported on members of the Chenopodiaceae and on Amaranthus. Disease symptoms: Infected leaves and petioles of B. vulgaris exhibit numerous circular leaf spots that coalesce in severe cases causing complete leaf collapse. Dark specks within a grey spot centre are characteristic for the disease. Older leaves exhibit a greater number of lesions with larger spot diameter. During the latter stage of severe epiphytotics, new leaf growth can be seen emerging from the plant surrounded by prostrate, collapsed leaves. Control: Fungicides in the benzimidazole and triazole class as well as organotin derivatives and strobilurins have successfully been used to control Cercospora leaf spot. Elevated levels of tolerance in populations of C. beticola to some of the chemicals registered for control has been documented. Partial genetic resistance also is used to reduce leaf spot disease.

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“…Later on families were produced with high yield and sucrose content, an acceptable degree of lignification, and bolting resistance (Schlosser, 1957 ;Schlosser & Koch, 1957 ;Campbell, 1966 ;Bilgen et al ., 1969 ;Lasa et al ., 1984) . Coe (1981) released highly resistant germplasm which was derived from a pool of polycross progenies from crosses made in the 1930s between sugar beets and garden beets .…”

Section: Fungal Diseasesmentioning

confidence: 99%