scholarly journals The bacterial impact on the transcriptional activity of DCL2 and DCL4 genes in wheat plants infected with Stagonospora nodorum

Biomics ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 343-351
Author(s):  
S.V. Veselova ◽  
G.F. Burkhanova ◽  
S.D. Rumyantsev ◽  
T.V. Nuzhnaya

Stagonospora nodorum Berk. is the causal agent of Septoria nodorum blotch (SNB) of wheat (Triticum aestivum L.). It synthesizes host-specific necrotrophic effectors (NEs), which facilitate infection process and ensure virulence of pathogen on host plant with a dominant susceptibility gene. The interaction of virulence genes products of the NEs pathogen (SnTox) with susceptibility genes products of the host plant (Snn) in the S. nodorum - wheat pathosystem is carried out in inverted gene-for-gene system and causes the development of disease. In this study, we tested three main NEs SnToxA, SnTox1, SnTox3, which have already been identified in S. nodorum at the gene level. The NEs role in the development of SNB has already been proven; however, the overall host response to SNB does not always strictly follow the inverted gene-for-gene system, as multiple SnTox-Snn interactions can be additive or epistatic. In this regard, the aim of the work was to identify the NE genes in three S. nodorum isolates and to study effect of NEs genes transcriptional activity on the isolate virulence. We have shown that all three NEs SnToxA, SnTox3 and SnTox1 played an important role in the development of the disease in compatible interactions. Effectors SnTox3 and SnTox1 exhibited epistatic interaction that was removed by a triple compatible interaction (SnTox3-Snn3, SnToxA-Tsn1 and SnTox1-Snn1). This effect was shown by us for the first time. The mechanisms of epistatic and additive interactions, as well as the virulence of the isolate were associated with the regulation of the NEs genes transcriptional activity. The avirulent isolate Sn4VD lacked transcription of all three NEs genes, and the virulent isolate Sn9MH was characterized by a high level of mRNA accumulation of all three NEs genes during infection on susceptible cultivar. We also showed that SnTox expression depended both on the host genotype in SnToxA and SnTox3 and on the number of compatible interactions exhibiting additive or epistatic interactions in SnTox1 and SnTox3. Finally, the virulence of the S. nodorum isolate depended on the qualitative and quantitative composition of NEs.


Author(s):  
Mikhail Yurievich Shein ◽  
Guzel Fanilevna Burkhanova ◽  
Anastasia Yurievna Merzlyakova ◽  
Igor Vladimirovich Maksimov

Biomics ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 352-358
Author(s):  
T.V. Nuzhnaya ◽  
S.V. Veselova ◽  
G.F. Burkhanova ◽  
S.D. Rumyantsev ◽  
I.V. Maksimov

The virulence of the causal agent of Septoria nodorum blotch of wheat pathogenic fungus Stagonospora nodorum Berk. is caused by the presence of necrotrophic effectors (SnTox). Isolates infect wheat varieties that carry susceptibility genes (Snn) corresponding to toxins in the genome. SnTox-Snn interactions are mirror images of classical gene-for-gene interactions and lead to the development of disease. In the present work, we have studied SnTox-Tsn1 and SnTox1-Snn1 interactions resulting in development of necrosis and chlorosis in wheat plant tissues with the formation of extensive lesions. It is assumed that the multiplicity of SnTox-Snn reactions can be carried out through the regulation of transcription of plant susceptibility genes. The aim of the work was to study the transcriptional activity of the Tsn1 and Snn1 susceptibility genes in wheat varieties with varying degrees of resistance to S. nodorum. Alleles of the Tsn1 and Snn1 susceptibility genes were identified by PCR in 12 varieties of winter and spring wheat. Seedling resistance was determined for all samples by the lawns method. Then five varieties were selected for further study. The resistance of the Omskaya 35 variety, which carries a single dominant Snn1 allele, was determined by the suppression of transcription of the Snn1 gene by almost 2 times. The resistance of the Yubileynaya 100 variety, which carries two dominant alleles Tsn1/Snn1, was determined by suppression of transcription of the Tsn1 gene by 8 times. The resistance of the Esaul and Yermak varieties, as well as the susceptibility of the Zhnitsa variety, were determined not only by the transcriptional activity of the Tsn1 gene, but possibly by other factors. A statistically significant positive correlation of 0.97 was found between the transcription level of the Tsn1 gene and the resistance of the variety.


2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.


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