scholarly journals Validation and Characterization of Maize Multiple Disease Resistance QTL

2019 ◽  
Vol 9 (9) ◽  
pp. 2905-2912 ◽  
Author(s):  
Lais B. Martins ◽  
Elizabeth Rucker ◽  
Wade Thomason ◽  
Randall J. Wisser ◽  
James B. Holland ◽  
...  
2008 ◽  
Vol 117 (4) ◽  
pp. 531-543 ◽  
Author(s):  
Young-Ki Jo ◽  
Reed Barker ◽  
William Pfender ◽  
Scott Warnke ◽  
Sung-Chur Sim ◽  
...  

Crop Science ◽  
2010 ◽  
Vol 50 (2) ◽  
pp. 458-466 ◽  
Author(s):  
Peter J. Balint-Kurti ◽  
Junyun Yang ◽  
George Van Esbroeck ◽  
Janelle Jung ◽  
Margaret E. Smith

2019 ◽  
Vol 117 (4) ◽  
pp. 617
Author(s):  
Anand C. Reddy ◽  
B. Lavanya ◽  
T. Tejaswi ◽  
E. Sreenivasa Rao ◽  
D. C. Lakshmana Reddy

2018 ◽  
Author(s):  
Sandeep R. Marla ◽  
Kevin Chu ◽  
Satya Chintamanani ◽  
Dilbag Multani ◽  
Antje Klempien ◽  
...  

ABSTRACTAdult plant resistance (APR) is an enigmatic phenomenon in which resistance genes are ineffective in protecting seedlings from disease but confer robust resistance at maturity. Maize has multiple cases in which genes confer APR to northern leaf spot, a lethal disease caused byCochliobolus carbonumrace 1 (CCR1). The first identified case of APR in maize is encoded by a hypomorphic allele,Hm1A, at thehm1locus. In contrast, wild type alleles ofhm1provide complete protection at all developmental stages and in every part of the maize plant.Hm1encodes an NADPH-dependent reductase, which inactivates HC-toxin, a key virulence effector of CCR1. Cloning and characterization ofHm1Aruled out differential transcription or translation for its APR phenotype and identified an amino acid substitution that reduced HC-toxin reductase (HCTR) activity. The possibility of a causal relationship between the weak nature ofHm1Aand its APR phenotype was confirmed by the generation of two new APR alleles ofHm1by mutagenesis. The HCTRs encoded by these new APR alleles had undergone relatively conservative missense changes that partially reduced their enzymatic activity similar to HM1A. No difference in accumulation of HCTR was observed between adult and juvenile plants, suggesting that the susceptibility of seedlings derives from a greater need for HCTR activity, not reduced accumulation of the gene product. Conditions and treatments that altered the photosynthetic output of the host had a dramatic effect on resistance imparted by the APR alleles, demonstrating a link between the energetic or metabolic status of the host and disease resistance affected by HC-toxin catabolism by the APR alleles of HCTR.AUTHOR SUMMARYAdult plant resistance (APR) is a phenomenon in which disease resistance genes are able to confer resistance at the adult stages of the plant but somehow fail to do so at the seedling stages. Despite the widespread occurrence of APR in various plant diseases, the mechanism underlying this trait remains obscure. It is not due to the differential transcription of these genes, and here we show that it is also not due to the differential translation or activity of the APR alleles of the maizehm1gene at different stages of development. Using a combination of molecular genetics, biochemistry and physiology, we present multiple lines of evidence that demonstrate that APR is a feature or symptom of weak forms of resistance. While the mature parts of the plant are metabolically robust enough to manifest resistance, seedling tissues are not, leaving them vulnerable to disease. Growth conditions that compromise the photosynthetic output of the plant further deteriorate the ability of the seedlings to protect themselves from pathogens.One sentence summaryCharacterization of adult plant resistance in the maize-CCR1 pathosystem reveals a causal link between weak resistance and APR.


2021 ◽  
Author(s):  
Dinesh Kumar Saini ◽  
Amneek Chahal ◽  
Neeraj Pal ◽  
Puja Srivast ◽  
Pushpendra Kumar Gupta

Abstract In wheat, meta-QTLs (MQTLs), and candidate genes (CGs) were identified for multiple disease resistance (MDR). For this purpose, information was collected from 58 studies for mapping QTLs for resistance to one or more of the five diseases. As many as 493 QTLs were available from these studies, which were distributed in five diseases as follows: septoria tritici blotch (STB) 126 QTLs; septoria nodorum blotch (SNB), 103; fusarium head blight (FHB), 184; karnal bunt (KB), 66, and loose smut (LS), 14. Of these 493 QTLs, only 291 QTLs could be projected onto a consensus genetic map, giving 63 MQTLs. The CI of the MQTLs ranged from 0.04 to 15.31 cM with an average of 3.09 cM per MQTL. This is a ~ 4.39 fold reduction from the CI of initial QTLs, which ranged from 0 to 197.6 cM, with a mean of 13.57 cM. Of 63 MQTLs, 60 were anchored to the reference physical map of wheat (the physical interval of these MQTLs ranged from 0.30 to 726.01 Mb with an average of 74.09 Mb). Thirty-eight (38) of these MQTLs were verified using marker-trait associations (MTAs) derived from genome-wide association studies. As many as 874 CGs were also identified which were further investigated for differential expression using data from five transcriptome studies, resulting in 194 differentially expressed genes (DEGs). Among the DEGs, 85 genes had functions previously reported to be associated with disease resistance. These results should prove useful for fine mapping of MDR genes and marker-assisted breeding.


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