Identification and molecular mapping of two soybean aphid resistance genes in soybean PI 587732

2014 ◽  
Vol 127 (5) ◽  
pp. 1251-1259 ◽  
Author(s):  
Ki-Seung Kim ◽  
Anitha Chirumamilla ◽  
Curtis B. Hill ◽  
Glen L. Hartman ◽  
Brian W. Diers
2008 ◽  
Vol 118 (3) ◽  
pp. 473-482 ◽  
Author(s):  
Guorong Zhang ◽  
Cuihua Gu ◽  
Dechun Wang

Author(s):  
S J Bhusal ◽  
R L Koch ◽  
A J Lorenz

Abstract Soybean aphid (Aphis glycines Matsumura (Hemiptera: Aphididae)) has been a major pest of soybean in North America since its detection in this continent in 2000 and subsequent spread. Although several aphid resistance genes have been identified, at least four soybean aphid biotypes have been discovered, with three of them being virulent on soybean cultivars with certain soybean aphid resistance genes. These biotypes are known to vary across years and locations, but information on their variation within single fields is limited. An investigation was conducted to study the variation of soybean aphid biotypes within single townships and fields in Minnesota. Screening of 28 soybean aphid isolates collected from seven soybean fields (six soybean fields in Cairo and Wellington Townships of Renville County, MN and one field in Wilmar Township of Kandiyohi County, MN) revealed the existence of multiple known biotypes of soybean aphid within single fields of soybean. We found up to three biotypes of soybean aphid in a single field. Two biotypes were found in five fields while only one field had only a single biotype. Three isolates presented reactions on a panel of resistant and susceptible indicator lines that were different from known biotypes. These results highlight the importance of characterizing soybean aphid biotypes in small geographical areas and utilizing generated knowledge to develop soybean cultivars pyramided with multiple resistance genes. The outcome will be decreased use of insecticides, thereby improving economic and environmental sustainability of soybean production.


2006 ◽  
Vol 19 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Yan Li ◽  
Curtis B. Hill ◽  
Shawn R. Carlson ◽  
Brian W. Diers ◽  
Glen L. Hartman

2013 ◽  
Vol 126 (8) ◽  
pp. 2081-2091 ◽  
Author(s):  
Carmille Bales ◽  
Guorong Zhang ◽  
Menghan Liu ◽  
Clarice Mensah ◽  
Cuihua Gu ◽  
...  

Crop Science ◽  
2005 ◽  
Vol 45 (6) ◽  
pp. 2273-2280 ◽  
Author(s):  
X. M. Liu ◽  
C. M. Smith ◽  
B. R. Friebe ◽  
B. S. Gill

2017 ◽  
Vol 130 (12) ◽  
pp. 2601-2615 ◽  
Author(s):  
Shichen Zhang ◽  
Zhongnan Zhang ◽  
Zixiang Wen ◽  
Cuihua Gu ◽  
Yong-Qiang Charles An ◽  
...  

2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  

Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.


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