Diversity among Greengram Germplasm to Powdery Mildew Resistance Caused by Erysiphe polygoni DC

Abstract Powdery mildew, Erysiphe polygoni DC, can be a significant problem on Hydrangea macrophylla (Thunb.) Ser. in the landscape in late summer to fall and during greenhouse propagation or production of potted plants. Because very little information related to sources of resistance is available, 90 H. macrophylla cultivars were evaluated for resistance to powdery mildew over a 3-year period. This included 69 H. macrophylla ssp. macrophylla and 18 H. macrophylla ssp. serrata (Thunb.) Makino cultivars, along with three cultivars that are hybrids between the two subspecies. Significant differences among cultivars to powdery mildew were found in all three study years. Three cultivars, ‘Amagi Amacha’, ‘Shirofuji’ and ‘Veitchii’, were among the most resistant each year. ‘Diadem’, ‘Komachi’, and ‘Omacha’ were highly resistant in 2006 and 2008, but only moderately resistant in 2007. ‘Komachi’ and ‘Shirofuji’ were considered unsuitable for breeding purposes as they do not appear to produce fertile flowers. ‘Veitchii’ was the only member of H. macrophylla ssp. macrophylla with a high level of powdery mildew resistance; while all other resistant cultivars were members of H. macrophylla ssp. serrata, not all members of this subspecies are resistant. Results of this study will be useful in breeding powdery mildew resistant H. macrophylla.

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Inheritance of Powdery Mildew Resistance in Sugar Beet Derived from Beta vulgaris subsp. maritima

Plant Disease ◽

10.1094/pdis.2001.85.6.627 ◽

2001 ◽

Vol 85 (6) ◽

pp. 627-631 ◽

Cited By ~ 25

Author(s):

R. T. Lewellen ◽

J. K. Schrandt

Keyword(s):

Powdery Mildew ◽

Sugar Beet ◽

Beta Vulgaris ◽

Powdery Mildew Resistance ◽

Major Gene ◽

Mildew Resistance ◽

Breeding Lines ◽

Erysiphe Polygoni ◽

Moderate Resistance ◽

High Level

Powdery mildew of sugar beet (Beta vulgaris), caused by Erysiphe polygoni, was introduced into North American in 1974. Since then, chemical control has been needed. Moderate resistance of a slow-mildewing type is known and has been used commercially. High resistance was identified recently in B. vulgaris subsp. maritima accessions WB97 and WB242 and has been backcrossed into sugar beet breeding lines. These enhanced lines were used as sources of powdery mildew resistance to determine the inheritance of resistance. Analyses of segregating testcross families showed that resistance from both sources is inherited as a single, dominant, major gene. The gene symbol Pm is proposed for the resistant allele. The allelism of the resistance from the two wild beet sources was not determined. Pm conditions a high level of resistance, but disease developed on matured leaves late in the season. This late development of mildew on lines and the slow-mildewing trait in susceptible, recurrent lines tended to obfuscate discrete disease ratings.

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Validation of molecular marker associated with powdery mildew resistance in mungbean

Indian Journal of Genetics and Plant Breeding (The) ◽

10.31742/ijgpb.78.3.17 ◽

2018 ◽

Vol 78 (3) ◽

Author(s):

Sumangala Bhat ◽

S. K. Pooja ◽

A. P. Sarkale

Keyword(s):

Powdery Mildew ◽

Ssr Markers ◽

Ssr Marker ◽

Powdery Mildew Resistance ◽

Phenotypic Variance ◽

Single Marker Analysis ◽

Mildew Resistance ◽

F2 Population ◽

Single Marker ◽

Erysiphe Polygoni

Powdery mildew caused by Erysiphe polygoni, is one of the major diseases of mungbean (Vigna radiata L. Wilczek), causes yield loss up to 20-40%. The present investigation was undertaken to study the SSR markers associated with powdery mildew resistance in mungbean. The resistant line, TARM1 was crossed with highly susceptible, but popular variety DGGV2 and the F1s were selfed to obtain F2. F2 population was evaluated for response to PM under field conditions. Of the 64 SSR markers studied, only four were found to be polymorphic between two parents (TARM1 and DGGV2). Single marker analysis indicated that one SSR marker (MB-SSR238) showed association with powdery mildew resistance in mungbean, explaining the phenotypic variance of 11.64%.

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