Geographic Distribution and Genetic Analysis of Physiological Racesof Setosphaeria turcica in Northern China

Abstract

Five hundreds and forty-six isolates of Setosphaeria turcica, the causal agent of Northern Corn Leaf Blight, were collected in 61 corn-growing locations throughout six provinces of Northern China during 2000-2002, to determine their pathogenicity on two sets of host differentials: OH43/Huangzao4, OH43Ht1Huangzao4Ht1, OH43Ht2/Huangzao4Ht2, OH43Ht3/Huangzao4Ht3 and OH43HtN/Huangzao4HtN. The isolates were grouped into 13 different physiological races (0, 1, 12, 3, 13, 23, N, 1N, 2N, 12N, 3N, 23N and 123N) based on their infection types on the host differentials. Incidence analyses indicated that races 0 and race 1 were still dominant in Northern China and took 40.66% and 18.32% of total isolates tested respectively, while other races sparsely occurred from 1.28-6.59%. The emergence of race 123N that was toxic to corn lines woth all four existing major resistant genes implies the possibility of present hybrids to loss their resistance in some regions of China. Further analysis of race distribution in Northern China demonstrated that the occurrence and composition of physiological races of S. turcica varied among provinces. Genetic analysis of within and between pathogenic race groups by random amplification polymorphic DNA (RAPD) markers revealed high genetic diversity in S. turcica population. Relatively high genetic similarity (70.46-95.12%) was identified within race groups and the results suggested that race groups were genetically similar within one geographic locations, but genetic migration could possibly happen between some locations which might lead to relative high genetic diversity within one geographic location. The similarity indexes derived from 13 race groups varied from 20.31 to 82.81% indicating great genetic variation between race groups. The UPGMA dendrograms generated by NTSys software grouped the 13 races into two not very robust but relatively distinct clusters: cluster I (0, 1, N, 12, 1N, 2N and 12N) and cluster II (3, 13, 23, 3N, 23N and 123N) with 63.7 and 72.3% P value respectively. The cluster analyses suggested that the pathogen might have a great genetic change while mutating to be virulent Ht3 resistant gene, but the details about the mechanisms were remain unaware.