Inheritance of resistance to the chlorosis component of tan spot of wheat caused by Pyrenophora tritici-repentis, races 1 and 3

Singh, Pawan K.; Hughes, G. R.

doi:10.1007/s10681-006-9229-x

Cited by 9 publications

(5 citation statements)

References 24 publications

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“…Tsc1 and Tsc2 genes ( Tan spot chlorosis ) sensitive for ToxC and ToxB ( Ciuffetti et al., 2014 ). Furthermore, several more genes have been recognized through conidial inoculations which are not associated with HSTs and have been named as ‘Tsr’ (Tan spot resistance) ( Singh and Hughes, 2006 ; Tadesse et al., 2006a ; Tadesse et al., 2006b ; McIntosh and Yamazaki, 2008 ; Singh et al., 2008 ). Toxin sensitivity was shown to be controlled by the Tsn1 gene ( Lamari and Bernier, 1989b ; Faris et al., 1996 ).…”

Section: Selected Fungal Pathogens On Grassesmentioning

confidence: 99%

“…Tsc1 and Tsc2 genes (Tan spot chlorosis) sensitive for ToxC and ToxB (Ciuffetti et al, 2014). Furthermore, several more genes have been recognized through conidial inoculations which are not associated with HSTs and have been named as 'Tsr' (Tan spot resistance) (Singh and Hughes, 2006;Tadesse et al, 2006a;Tadesse et al, 2006b;McIntosh and Yamazaki, 2008;Singh et al, 2008). Toxin (Lamari et al, 1995;Lamari et al, 1998;Ali and Francl, 2003;Singh, 2007;Aboukhaddour et al, 2013) and the Southern Cone Region of South America (Singh, 2007) Race 3 ToxC 3 North America (Lamari et al, 1998;Ali and Francl, 2003;Singh, 2007;Aboukhaddour et al, 2013) and the Caucasus region (Lamari et al, 2005) Race 4 No HTSs 4 North America (Lamari et al, 1995;Lamari et al, 1998;Ali and Francl, 2003;Singh, 2007;Aboukhaddour et al, 2013) and North Africa (Benslimane et al, 2011) Race 5…”

Section: Pyrenophora Tritici-repentismentioning

confidence: 99%

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Fungal Pathogens in Grasslands

Karunarathna

Tibpromma

Jayawardena

et al. 2021

Front. Cell. Infect. Microbiol.

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Grasslands are major primary producers and function as major components of important watersheds. Although a concise definition of grasslands cannot be given using a physiognomic or structural approach, grasslands can be described as vegetation communities experiencing periodical droughts and with canopies dominated by grasses and grass-like plants. Grasslands have a cosmopolitan distribution except for the Antarctic region. Fungal interactions with grasses can be pathogenic or symbiotic. Herbivorous mammals, insects, other grassland animals, and fungal pathogens are known to play important roles in maintaining the biomass and biodiversity of grasslands. Although most pathogenicity studies on the members of Poaceae have been focused on economically important crops, the plant-fungal pathogenic interactions involved can extend to the full range of ecological circumstances that exist in nature. Hence, it is important to delineate the fungal pathogen communities and their interactions in man-made monoculture systems and highly diverse natural ecosystems. A better understanding of the key fungal players can be achieved by combining modern techniques such as next-generation sequencing (NGS) together with studies involving classic phytopathology, taxonomy, and phylogeny. It is of utmost importance to develop experimental designs that account for the ecological complexity of the relationships between grasses and fungi, both above and below ground. In grasslands, loss in species diversity increases interactions such as herbivory, mutualism, predation or infectious disease transmission. Host species density and the presence of heterospecific host species, also affect the disease dynamics in grasslands. Many studies have shown that lower species diversity increases the severity as well as the transmission rate of fungal diseases. Moreover, communities that were once highly diverse but have experienced decreased species richness and dominancy have also shown higher pathogenicity load due to the relaxed competition, although this effect is lower in natural communities. This review addresses the taxonomy, phylogeny, and ecology of grassland fungal pathogens and their interactions in grassland ecosystems.

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Section: Selected Fungal Pathogens On Grassesmentioning

confidence: 99%

Section: Pyrenophora Tritici-repentismentioning

confidence: 99%

Fungal Pathogens in Grasslands

Karunarathna

Tibpromma

Jayawardena

et al. 2021

Front. Cell. Infect. Microbiol.

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“…Genetic analysis of wheat- P. tritici-repentis interactions have revealed that host resistance ranges from qualitative [10,11,12,13,14] to quantitative control [15,16,17,18,19,20]. Some studies utilizing quantitative trait loci (QTL) analysis reported resistance to TS as polygenic, but observed that previously reported major genes frequently underline these QTLs [18,20,21].…”

Section: Introductionmentioning

confidence: 99%

Characterization of QTLs for Seedling Resistance to Tan Spot and Septoria Nodorum Blotch in the PBW343/Kenya Nyangumi Wheat Recombinant Inbred Lines Population

Singh

Deng

et al. 2019

IJMS

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Tan spot (TS) and Septoria nodorum blotch (SNB) induced by Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively, cause significant yield losses and adversely affect grain quality. The objectives of this study were to decipher the genetics and map the resistance to TS and SNB in the PBW343/Kenya Nyangumi (KN) population comprising 204 F6 recombinant inbred lines (RILs). Disease screening was performed at the seedling stage under greenhouse conditions. TS was induced by P. tritici-repentis isolate MexPtr1 while SNB by P. nodorum isolate MexSN1. Segregation pattern of the RILs indicated that resistance to TS and SNB in this population was quantitative. Diversity Array Technology (DArTs) and simple sequence repeats (SSRs) markers were used to identify the quantitative trait loci (QTL) for the diseases using inclusive composite interval mapping (ICIM). Seven significant additive QTLs for TS resistance explaining 2.98 to 23.32% of the phenotypic variation were identified on chromosomes 1A, 1B, 5B, 7B and 7D. For SNB, five QTLs were found on chromosomes 1A, 5A, and 5B, explaining 5.24 to 20.87% of the phenotypic variation. The TS QTL on 1B chromosome coincided with the pleiotropic adult plant resistance (APR) gene Lr46/Yr29/Pm39. This is the first report of the APR gene Lr46/Yr29/Pm39 contributing to TS resistance.

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“…The mode of inheritance of resistance to chlorosis also varied from recessive, through partially dominant to dominant depending upon the parental genotypes (Singh and Hughes 2006b). Moreover, the expression of tan spot chlorotic symptom is continuous and highly influenced by environment (Singh and Hughes 2006b). The germplasm used in this study showed contrasting high levels of resistance and susceptibility and discrete differences in reaction permitted a showing the location of gene Tsr1 for resistance to tan spot and insensitivity to culture filtrate of Pyrenophora tritici-repentis race 2.…”

Section: Disease Score Ril Frequencymentioning

confidence: 90%

“…However, Singh et al (2008a) observed that resistance to race 5 was controlled by a single dominant gene whereas Friesen and Faris (2004) reported resistance to be quantitative with the toxin-insensitivity gene, Tsc2, mapping to the distal region of chromosome 2BS accounting for 69% of the phenotypic variation. The mode of inheritance of resistance to chlorosis also varied from recessive, through partially dominant to dominant depending upon the parental genotypes (Singh and Hughes 2006b). Moreover, the expression of tan spot chlorotic symptom is continuous and highly influenced by environment (Singh and Hughes 2006b).…”

Section: Disease Score Ril Frequencymentioning

confidence: 99%

Genetic and molecular analysis of wheat tan spot resistance effective against Pyrenophora tritici-repentis races 2 and 5

et al. 2009

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Tan spot, a major foliar disease of wheat (Triticum aestivum L.), is caused by an ascomycete Pyrenophora tritici-repentis. Both culture filtrates and conidiospore inocula induce disease symptoms in susceptible wheat genotypes. The objectives of this study were to determine and map the genetic control of resistance to spore inocula and culture filtrates of P. tritici-repentis races 2 and 5. The F 1 and F 2 generations and an F 2:6 recombinant inbred lines (RIL) population were developed from a cross between the resistant ND 735 and the susceptible Steele-ND. Disease assessments of the segregating generations were done at the seedling stage using culture filtrates and spore inocula under controlled environmental conditions. Genetic and mapping analyses of the F 1 and F 2 generations and the RIL by both methods indicated that the same single recessive gene, Tsr1, located on chromosome 5BL, controlled resistance and insensitivity to necrosis induced by race 2. A second recessive gene, designated Tsr6, located on chromosome 2BS, conferred resistance/insensitivity to chlorosis induced by spore inocula or culture filtrates of race 5. Diversity Arrays Technology markers wPt-3049 (2.9 cM) and wPt-0289 (4.6 cM) were closely linked to Tsr1 and Tsr6, respectively. The results further indicated that culture filtrates can be used as surrogates for spore inoculation. Tsr1 and Tsr6 can be selected by marker-assisted selection in breeding for resistance to tan spot.

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Inheritance of resistance to the chlorosis component of tan spot of wheat caused by Pyrenophora tritici-repentis, races 1 and 3

Cited by 9 publications

References 24 publications

Fungal Pathogens in Grasslands

Fungal Pathogens in Grasslands

Characterization of QTLs for Seedling Resistance to Tan Spot and Septoria Nodorum Blotch in the PBW343/Kenya Nyangumi Wheat Recombinant Inbred Lines Population

Genetic and molecular analysis of wheat tan spot resistance effective against Pyrenophora tritici-repentis races 2 and 5

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