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Review
. 2023 Mar 29:14:1023824.
doi: 10.3389/fpls.2023.1023824. eCollection 2023.

Genetics and breeding for resistance against four leaf spot diseases in wheat (Triticum aestivum L.)

Pushpendra Kumar Gupta  1   2   3 , Neeraj Kumar Vasistha  1   4 , Sahadev Singh  1 , Arun Kumar Joshi  3   5
Affiliations
Review

Genetics and breeding for resistance against four leaf spot diseases in wheat (Triticum aestivum L.)

Pushpendra Kumar Gupta et al. Front Plant Sci. .

Abstract

In wheat, major yield losses are caused by a variety of diseases including rusts, spike diseases, leaf spot and root diseases. The genetics of resistance against all these diseases have been studied in great detail and utilized for breeding resistant cultivars. The resistance against leaf spot diseases caused by each individual necrotroph/hemi-biotroph involves a complex system involving resistance (R) genes, sensitivity (S) genes, small secreted protein (SSP) genes and quantitative resistance loci (QRLs). This review deals with resistance for the following four-leaf spot diseases: (i) Septoria nodorum blotch (SNB) caused by Parastagonospora nodorum; (ii) Tan spot (TS) caused by Pyrenophora tritici-repentis; (iii) Spot blotch (SB) caused by Bipolaris sorokiniana and (iv) Septoria tritici blotch (STB) caused by Zymoseptoria tritici.

Keywords: PR proteins; necrotrophic effectors; pathogens; resistance genes; sensitivity genes; wheat.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The visual symptoms of four necrotrophic and hemibiotrophic diseases. (A) SNB; (B) TS (B.1 and B.2 showing necrosis and chlorosis); (C) SB and (D) STB.
Figure 2
Figure 2
Two different models for host- pathogen interactions in plants: (A) gene-for gene (GFG) model, proposed by Flor (1956) and (B) an inverse gene-for gene (IGFG) model that was discovered recently in a number of necrotrophic diseases in wheat.
Figure 3
Figure 3
Major molecular events during Z. tritici–wheat interactions. (A) Fungal PAMP chitin is recognized by the host receptors Chitin Elicitor Binding Protein (CEBiP) and Chitin Elicitor Receptor Kinase 1 (CERK1), triggering MAP kinase cascades and immune activation. Multi-functional LysM-domain containing effector Mg3LysM scavenges chitin to suppress immunity and protects fungal hyphae from wheat chitinases. (B) ’Necrotrophic’ effectors (NEs), Necrosis-Inducing Protein 1/2 (ZtNIP1/2) and and LysM effector (Zt3LysM) induce host cell death. (C) Stb gene-specified resistance, presumably triggered following recognition of cognate fungal effectors (AvrStb) secreted into the apoplast. This results in arrest of pathogen growth via an unknown mechanism that does not involve HR. (D) The NEP1-like effector protein MgNLP (unknown Z. triticini effector, predicted by bioinformatics analysis) has an unknown function(s) during wheat infection, but triggers cell death in dicots. (E) Small secreted proteins (ZtSSPs) of Z. tritici, which act as an effector. The TaE3UBQ synthesize in the wheat and interacts with the ZtSSPs resulting inhibition of the growth of Z. tritici pathogen.
Figure 4
Figure 4
A schematic figure which shows a holistic view of the management of four foliar diseases through genetic tools.
See this image and copyright information in PMC

References

    1. Abeysekara N. S., Faris J. D., Chao S., McClean P. E., Friesen T. L. (2012). Whole-genome QTL analysis of stagonospora nodorum blotch resistance and validation of the SnTox4-Snn4 interaction in hexaploid wheat. Phytopathology 102, 94–104. doi: 10.1094/PHYTO-02-11-0040 - DOI - PubMed
    1. Adhikari T. B., Jackson E. W., Gurung S., Hansen J. M., Bonman J. M. (2011). Association mapping of quantitative resistance to Phaeosphaeria nodorum in spring wheat landraces from the USDA national small grains collection. Phytopathology 101, 1301–1310. doi: 10.1094/PHYTO-03-11-0076 - DOI - PubMed
    1. Adhikari T. B., Mamidi S., Gurung S., Bonman J. M. (2015). Mapping of new quantitative trait loci (QTL) for resistance to septoria tritici blotch in spring wheat (Triticum aestivum l.). Euphytica 205, 699–706. doi: 10.1007/s10681-015-1393-4 - DOI
    1. Aggarwal R., Agarwal S., Sharma S., Gurjar M. S., Bashyal B. M., Rao A. R., et al. . (2022). Whole-genome sequence analysis of Bipolaris sorokiniana infecting wheat in India and characterization of ToxA gene in different isolates as pathogenicity determinants. 3 Biotech. 12, 151. doi: 10.1007/s13205-022-03213-3 - DOI - PMC - PubMed
    1. Aggarwal R., Sharma S., Singh K., Gurjar M. S., Saharan M. S., Gupta S., et al. . (2019). First draft genome sequence of wheat spot blotch pathogen Bipolaris sorokiniana BS_112 from India, obtained using hybrid assembly. Microbiol. Res. Announc. 8, e00308–e00319. doi: 10.1128/MRA.00308-19 - DOI - PMC - PubMed

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