scholarly journals Pyrenophora tritici-repentis, Causal Agent of Tan Spot: A Review of Intraspecific Genetic Diversity

Author(s):  
M. V. ◽  
S. A. ◽  
A. E.
Plant Disease ◽  
2021 ◽  
Author(s):  
Marwa Laribi ◽  
Alireza Akhavan ◽  
Sarrah M'Barek ◽  
Amor Yahyaoui ◽  
Stephen Ernest Strelkov ◽  
...  

Pyrenophora tritici-repentis (Ptr) causes tan spot, an important foliar disease of wheat. A collection of Ptr isolates from Tunisia, located in one of the main secondary centers of diversification of durum wheat, was tested for phenotypic race classification based on virulence on a host differential set, and for the presence of the necrotrophic effector (NE) genes ToxA, ToxB , and toxb by PCR analysis. While races 2, 4, 5, 6, 7, and 8 were identified according to their virulence phenotypes, PCR testing indicated the presence of ‘atypical’ isolates that induced necrosis on the wheat differential ‘Glenlea’, but lacked the expected ToxA gene, suggesting the involvement of other NEs in the Ptr/wheat interaction. Genetic diversity and the Ptr population structure were explored further by examining 59 Tunisian isolates and 35 isolates from Algeria, Azerbaijan, Canada, Iran, and Syria using 24 simple sequence repeat markers. Average genetic diversity, overall gene flow and percentage polymorphic loci were estimated as 0.58, 2.09 and 87%, respectively. Analysis of molecular variance showed that 81% of the genetic variance occurred within populations and 19% between populations. Cluster analysis by the unweighted pair group method indicated that ToxB- isolates grouped together and were distantly related to ToxB+ isolates. Based on Nei’s analysis, the global collection clustered into two distinct groups according to their region of origin. The results suggest that both geographic origin and the host-specificity imposed by different NEs can lead to differentiation among Ptr populations.


2003 ◽  
Vol 81 (8) ◽  
pp. 890-895 ◽  
Author(s):  
T L Friesen ◽  
S Ali ◽  
R W Stack ◽  
L J Francl ◽  
J B Rasmussen

Laboratory conditions were identified for efficient production of the teleomorph of Pyrenophora tritici-repentis, causal agent of tan spot of wheat. Ascopcarp density (pseudothecia/cm2) and timing of ascospore maturity and discharge were determined for the fungus incubated on green or senescent maize leaves under various light regimes at 15 °C. The most rapid ascospore maturity (20 days) and discharge (26 days) occurred in a 12-h photoperiod on green leaves. However, incubation in continuous darkness increased ascocarp density. Rapid and efficient ascospore production was obtained by incubating the fungus on senescent leaves in continuous darkness for 12 days followed by a 12-h photoperiod. This resulted in ascospore discharge in 29 days from a high density of pseudothecia. Further, 95% of pseudothecia sampled contained mature ascospores at the time of first discharge. The maximum ascospore discharge height observed was 8.8 cm. Pseudothecial neck development was positively phototropic.Key words: Drechslera, ascomycete, loculascomycete, tan spot, ascospore, pseudothecium


Author(s):  
Noureddine Ouaar ◽  
Abdelkader Benbelkacem ◽  
Pawan Kumar Singh ◽  
Sabrina Oumata ◽  
Hamida Benslimane

2006 ◽  
Vol 96 (8) ◽  
pp. 885-889 ◽  
Author(s):  
P. K. Singh ◽  
J. L. Gonzalez-Hernandez ◽  
M. Mergoum ◽  
S. Ali ◽  
T. B. Adhikari ◽  
...  

Race 3 of the fungus Pyrenophora tritici-repentis, causal agent of tan spot, induces differential symptoms in tetraploid and hexaploid wheat, causing necrosis and chlorosis, respectively. This study was conducted to examine the genetic control of resistance to necrosis induced by P. tritici-repentis race 3 and to map resistance genes identified in tetraploid wheat (Triticum turgidum). A mapping population of recombinant inbred lines (RILs) was developed from a cross between the resistant genotype T. tur-gidum no. 283 (PI 352519) and the susceptible durum cv. Coulter. Based on the reactions of the Langdon-T. dicoccoides (LDN[DIC]) disomic substitution lines, chromosomal location of the resistance genes was determined and further molecular mapping of the resistance genes for race 3 was conducted in 80 RILs of the cross T. turgidum no. 283/Coulter. Plants were inoculated at the two-leaf stage and disease reaction was assessed 8 days after inoculation based on lesion type. Disease reaction of the LDN(DIC) lines and molecular mapping on the T. turgidum no. 283/Coulter population indicated that the gene, designated tsn2, conditioning resistance to race 3 is located on the long arm of chromosome 3B. Genetic analysis of the F2 generation and of the F4:5 and F6:7 families indicated that a single recessive gene controlled resistance to necrosis induced by race 3 in the cross studied.


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