Fungal pathogens deploy a barrage of secreted effectors to subvert host immunity, often by evading, disrupting, or altering key components of transcription, defense signaling, and metabolic pathways. However, the underlying mechanisms of effectors and their host targets are largely unexplored in necrotrophic fungal pathogens. Here, we describe the effector protein Ascochyta rabiei PEXEL-like Effector Candidate 25 (ArPEC25), which is secreted by the necrotroph A. rabiei, the causal agent of Ascochyta blight disease in chickpea (Cicer arietinum), and is indispensable for virulence. After entering host cells, ArPEC25 localizes to the nucleus and targets the host LIM transcription factor CaβLIM1a. CaβLIM1a is a transcriptional regulator of CaPAL1, which encodes phenylalanine ammonia lyase (PAL), the regulatory, gatekeeping enzyme of the phenylpropanoid pathway. ArPEC25 inhibits the transactivation of CaβLIM1a by interfering with its DNA-binding ability, resulting in negative regulation of the phenylpropanoid pathway and decreased levels of intermediates of lignin biosynthesis, thereby suppressing lignin production. Our findings illustrate the role of fungal effectors in enhancing virulence by targeting a key defense pathway that leads to the biosynthesis of various secondary metabolites and antifungal compounds. This study provides a template for the study of less explored necrotrophic effectors and their host target functions.

The corm rot of saffron caused by Fusarium oxysporum (Fox) has been reported to be the most destructive fungal disease of the herb globally. The pathogen, Fusarium oxysporum R1 (Fox R1) isolated by our group from Kashmir, India, was found to be different from Fusarium oxysporum f.sp. gladioli commonly reported corm rot agent of saffron. In the present study, Fox R1 was further characterized using housekeeping genes and pathogenicity tests, as Fusarium oxysporum R1 f.sp. iridacearum race 4. Though Fox R1 invaded the saffron plant through both corm and roots, the corm was found to be the preferred site of infection. In addition, the route of pathogen movement wastracked by monitoring visual symptoms, semi-quantitative PCR, quantitative-PCR (q-PCR), real-time imaging of egfp-tagged Fusarium oxysporum R1, and Fox R1 load quantification. This study is the first study of its kind on the bidirectional pathogenesis from corm to roots and vice-versa, as the literature only reports unidirectional upward movement from roots to other parts of the plant. In addition, the colonization pattern of Fox R1 in saffron corms and roots was studied. The present study involved a systematic elucidation of the mode and mechanism of pathogenesis in the saffron Fusarium oxysporum strain R1 pathosystem.

Background: Anti-inflammatory effects of statins have generated maximum interest, as has been demonstrated in a number of studies showing rapid decrease in CRP levels in patients of acute coronary syndromes. This CRP lowering property of statins has also translated into clinical benefits as suggested by reduction in rate of recurrent angina, recurrent myocardial infarction, and mortality.Methods: This prospective, open, and controlled study was conducted on 160 indoor and outdoor patients, for total duration of two years (2005-2006), in GMC Bhopal, MP, India.Results: In all the four groups, baseline serum hs-CRP was statistically significant (p value <0.01) higher than normal hs-CRP level. Mean reduction (%) in hs-CRP after 3 months of statin therapy was 83.6% in group A and 62.4% in group C which is highly significant (p value <0.001). In group B also, 26% hs-CRP reduction was noticed which is statistically significant (p value <0.01). Baseline hs-CRP was statistically significant high (p value <0.01) in hypertensive patients. Percentages reduction in group A (87%) and group C (66%) was statistically significant (p value <0.01). Baseline hs-CRP was statistically significant higher (p value <0.01) than normal population. After 3 months of statin therapy percentage reduction in group A and group C was statistically significant (p value <0.01). Conclusions: Low dose atorvastatin can significantly reduce CRP level in patients with risk factors for cardiovascular disease. Early initiation of low dose atorvastatin can reduce this inflammatory marker in both ACS and high risk for ACS patients and can prevent major adverse cardiac events.