Fine mapping of the SCN resistance QTL cqSCN-006 and cqSCN-007 from Glycine soja PI 468916

Euphytica ◽  
2017 ◽  
Vol 213 (2) ◽  
Author(s):  
Neil Yu ◽  
Brian W. Diers
Author(s):  
Katelyn Butler ◽  
Christina Fliege ◽  
Ryan Zapotocny ◽  
Brian Diers ◽  
Mathew Hudson ◽  
...  

Soybean cyst nematode is the most economically damaging pathogen of soybean and host resistance is a core management strategy. The SCN resistance QTL cqSCN-006, introgressed from the wild relative Glycine soja, provides intermediate resistance against nematode populations including those with increased virulence on the heavily used rhg1-b resistance locus. cqSCN-006 was previously fine-mapped to a genome interval on chromosome 15. The present study determined that Glyma.15G191200 at cqSCN-006, encoding a ɣ-SNAP (gamma-SNAP), contributes to SCN resistance. CRISPR/Cas9-mediated disruption of the cqSCN-006 allele reduced SCN resistance in transgenic roots. There are no encoded amino acid polymorphisms between resistant and susceptible alleles. However, other cqSCN-006-specific DNA polymorphisms in the Glyma.15G191200 promoter and gene body were identified, and we observed differing induction of ɣ-SNAP protein abundance at SCN infection sites between resistant and susceptible roots. We identified alternative RNA splice forms transcribed from the Glyma.15G191200 ɣ-SNAP gene and observed differential expression of the splice forms two days after SCN infection. Heterologous overexpression of ɣ-SNAPs in plant leaves caused moderate necrosis, suggesting that careful regulation of this protein is required for cellular homeostasis. Apparently, certain G. soja evolved quantitative SCN resistance through altered regulation of ɣ-SNAP. Previous work has demonstrated SCN resistance impacts of the soybean α-SNAP proteins encoded by Glyma.18G022500 (Rhg1) and Glyma.11G234500. The present study shows that a different type of SNAP protein can also impact SCN resistance. Little is known about ɣ-SNAPs in any system, but the present work suggests a role for ɣ-SNAPs during susceptible responses to cyst nematodes.


Crop Science ◽  
2006 ◽  
Vol 46 (3) ◽  
pp. 1094-1099 ◽  
Author(s):  
S. Zhu ◽  
D. R. Walker ◽  
H. R. Boerma ◽  
J. N. All ◽  
W. A. Parrott

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yuanyuan Zhao ◽  
Yiwei Liu ◽  
Zhenghai Zhang ◽  
Yacong Cao ◽  
Hailong Yu ◽  
...  

2006 ◽  
Vol 86 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Shawn M. J Winter ◽  
Istvan Rajcan ◽  
Barry J Shelp

Soybean cyst nematode (SCN) is the primary pest responsible for yield losses of Glycine max. Management of SCN remains difficult in commercial soybean production due to the length of its biological cycle, frequent changes in population virulence, and ease of spread via infested soil. Effective management relies on crop rotation in combination with resistant cultivars, which have been derived from a limited germplasm base. Breeding for SCN resistance in soybean is difficult due to the quantitative nature of the trait, genetic variation within SCN populations, time required for phenotyping experimental soybean lines, and environmental factors affecting SCN reproduction. Quantitative trait loci associated with SCN resistance have been identified on 17 of the 20 soybean linkage groups, explaining 1–91% of the total phenotypic variation. Two major resistance genes, rhg 1 and Rhg 4, have been identified on linkage groups G and A2, respectively. Several minor resistance genes have been identified, but their importance varies with germplasm source and nematode race. Enhancement of SCN resistance in G. max may be achieved by interspecific hybridization with G. soja, the wild ancestor, or by engineering plants with candidate resistance genes such as Hs1pro-1. Key words: Genetic engineering, Glycine soja, soybean cyst nematode, molecular markers, resistance


2019 ◽  
Vol 132 (7) ◽  
pp. 2039-2053 ◽  
Author(s):  
Barbara Steiner ◽  
Maria Buerstmayr ◽  
Christian Wagner ◽  
Andrea Danler ◽  
Babur Eshonkulov ◽  
...  

2017 ◽  
Vol 130 (9) ◽  
pp. 1941-1952 ◽  
Author(s):  
Shichen Zhang ◽  
Zhongnan Zhang ◽  
Carmille Bales ◽  
Cuihua Gu ◽  
Chris DiFonzo ◽  
...  

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

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Janice Kofsky ◽  
Hengyou Zhang ◽  
Bao-Hua Song

AbstractSoybean cyst nematode (SCN, Heterodera glycine Ichinohe) is the most damaging soybean pest worldwide and management of SCN remains challenging. The current SCN resistant soybean cultivars, mainly developed from the cultivated soybean gene pool, are losing resistance due to SCN race shifts. The domestication process and modern breeding practices of soybean cultivars often involve strong selection for desired agronomic traits, and thus, decreased genetic variation in modern cultivars, which consequently resulted in limited sources of SCN resistance. Wild soybean (Glycine soja) is the wild ancestor of cultivated soybean (Glycine max) and it’s gene pool is indisputably more diverse than G. max. Our aim is to identify novel resistant genetic resources from wild soybean for the development of new SCN resistant cultivars. In this study, resistance response to HG type 2.5.7 (race 5) of SCN was investigated in a newly identified SCN resistant ecotype, NRS100. To understand the resistance mechanism in this ecotype, we compared RNA seq-based transcriptomes of NRS100 with two SCN-susceptible accessions of G. soja and G. max, as well as an extensively studied SCN resistant cultivar, Peking, under both control and nematode J2-treated conditions. The proposed mechanisms of resistance in NRS100 includes the suppression of the jasmonic acid (JA) signaling pathway in order to allow for salicylic acid (SA) signaling-activated resistance response and polyamine synthesis to promote structural integrity of root cell walls. Our study identifies a set of novel candidate genes and associated pathways involved in SCN resistance and the finding provides insight into the mechanism of SCN resistance in wild soybean, advancing the understanding of resistance and the use of wild soybean-sourced resistance for soybean improvement.


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