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Tilletia indica causes the disease Karnal bunt in wheat. The disease is under international quarantine regulations. Comparative mitochondrial (mt) genome analysis of T. indica (KX394364 and DQ993184) and T. walkeri (EF536375) has found 325 to 328 SNPs, 57 to 60 short InDels (from 1 to 13 nt), two InDels (30 and 61 nt) and five (>200 nt) presence/absence variations (PAVs) between the two species. The mt genomes of both species have identical gene order. The numbers of SNPs and InDels between the mt genomes of the two species are approximately nine times of the corresponding numbers between the two T. indica isolates. There are eight SNPs between T. indica and T. walkeri that resulted in amino acid substitutions in the mt genes of cob, nad2 and nad5. In contrast, there is no amino acid substitution in the mt genes of the T. indica isolates from the SNPs found. The five PAVs present in T. indica (DQ993184) are absent in T. walkeri. Four PAVs are more than 1 kb and are not present in every T. indica isolate. Analysis of their presence and absence separates a collection of T. indica isolates into 11 subgroups. Two PAVs have ORFs for the LAGLIDAG endonuclease and two have ORFs for the GIY-YIG endonuclease family, which are representatives of homing endonuclease genes (HEGs). These intron- encoded HEGs confer intron mobility and account for their fluid distribution in T. indica isolates. The small PAV of 221 bp, present in every T. indica isolate and unique to the species, was used as the genetic fingerprint for the successful development of a rapid, highly sensitive and specific loop mediated isothermal amplification (LAMP) assay. The simple procedure of the LAMP assay and the easy detection formats will enable the assay to be automated for high throughput diagnosis. [ABSTRACT FROM AUTHOR]

Karnal bunt of wheat caused by Tilletia indica can be a hindrance to wheat trade as the fungal disease is known to affect the quality of the grain. As a breeding strategy, a set of eight near isogenics lines (NILs) and backcross derived recombinant inbred lines (micro-RILs) were developed in the background of PBW 343 and WH542 for Karnal bunt resistance over a period of time. The donor stocks resistant to Karnal bunt used in the study were ALDAN 'S' / IAS 58, CMH 77.308, H567.7I, HD29, HP1531, W485 and their derived lines KBRL 22 and KBRL 57. Effective method for screening to Karnal bunt was standardized and used for identification of resistant lines across many seasons. Some of the identified lines evaluated for yield were found to be equivalent to the high yielding parents and the commercially grown check varieties. These developed lines will serve as a basic material for production of Karnal bunt free wheat. [ABSTRACT FROM AUTHOR]

Tilletia indica Mitra, the causal agent of Karnal bunt of wheat (KB), is a quarantined disease of international importance whose pathogen shows high variability due to its heterothallic nature. Pathogenic variation was studied under artificially inoculated conditions on 13 wheat genotypes including bread and dicoccum wheat. This study used 34 T. indica isolates collected from 6 major wheat growing states in India (Rajasthan, Haryana, Punjab, Himachal Pradesh, Uttarakhand, and Uttar Pradesh). Mean coefficient of infection of the isolates ranged from 2.11% (KBR4) to 14.60% (KBH1). Among the 13 genotypes screened, only 1 genotype was found to be highly susceptible to infection. KBR1 and KBHP3 were the most virulent and least aggressive isolates and had coefficients of infection of 79.42% and 6.22%, respectively, on the susceptible variety HD 2009. Pathogenic variability test revealed the existence of 3 different aggressive groups among the 34 selected isolates on a set of host differentials. A total of 64 monosporidial (Ms) lines were developed from the isolates, which originated from 6 states, representing 19 locations in the North Western plains zone of India. Self-paired Ms lines revealed 2 mating alleles. A total of 15 mating alleles were postulated using 46 Ms lines. This study confirmed the heterothallic nature of T. indica and the existence of multiple alleles controlling pathogenicity. [ABSTRACT FROM AUTHOR]

Two wheat varieties, one highly resistant (HD29) and another susceptible (WH542) and their recombinant lines were taken for expression profiling of cystatins at three stages (WS1, WS2 and WS3) of the developing spikes. Different biochemical and immunological techniques like protease inhibitor assay, ELISA, DOT-BLOT immunoassay and SDS-PAGE analysis were employed to reveal the relationship of cystatin expression with stage dependent resistance (P<0.01). Interestingly, in all the genotypes cystatin expression was the highest at WS2 stage which is most susceptible to Karnal bunt (KB) pathogen. Expression was higher in the resistant recombinant inbred lines than in the susceptible ones (P<0.0001). Percent disease severity results were also in accordance with cystatin expression studies and thus suggesting a direct role of cystatins in providing resistance against KB. Based on the presence of potential component markers like cystatins which are involved in defence, identification of resistant wheat germplasms can prove to be an important strategy for successful KB management. [ABSTRACT FROM AUTHOR]

Karnal bunt (KB) of wheat, caused by the fungus Tilletia indica, is a challenge to the grain industry, owing not to direct yield loss but to quarantine regulations that may restrict international movement of affected grain. Several different sources of resistance to KB have been reported. Understanding the genetics of resistance will facilitate the introgression of resistance into new wheat cultivars. The objectives of this study were to identify quantitative trait loci (QTLs) associated with KB resistance and to identify DNA markers in two recombinant inbred line populations derived from crosses of the susceptible cultivar WH542 with resistant lines HD29 and W485. Populations were evaluated for resistance against the KB pathogen for 3 years at Punjab Agricultural University, Ludhiana, India. Two new QTLs ( Qkb.ksu-5BL.1 and Qkb.ksu-6BS.1) with resistance alleles from HD29 were identified and mapped in the intervals Xgdm116– Xwmc235 on chromosome 5B (deletion bin 5BL9-0.76-0.79) and Xwmc105– Xgwm88 on chromosome 6B (C-6BS5-0.76). They explained up to 19 and 13% of phenotypic variance, respectively. Another QTL ( Qkb.ksu-4BL.1) with a resistance allele from W485 mapped in the interval Xgwm6– Xwmc349 on chromosome 4B (4BL5-0.86-1.00) and explained up to 15% of phenotypic variance. Qkb.ksu-6BS.1 showed pairwise interactions with loci on chromosomes 3B and 6A. Markers suitable for marker-assisted selection are available for all three QTLs. [ABSTRACT FROM AUTHOR]