(R2022) Mathematical Modelling of Tuberculosis and COVID-19 Co-infection in India: A Real Data Analysis on Concomitant Diseases

In this paper, we have proposed an epidemiological model to study the dynamics of two concomitant diseases Tuberculosis (TB) and COVID-19. Here, we have formulated a deterministic compartmental model as an extended form of the classical SIS model. First, the basic reproduction number R0 is derived and then stability analysis of the model is done. It is observed that the disease-free equilibrium is stable when R0 is less than one and the endemic equilibrium is stable only when R0 is greater than one. Numerical simulation is carried out to illustrate the theoretical findings and to study the transmission dynamics of both the concomitant diseases during the first and second waves of COVID-19 in India

Proteomic changes associated with deletion of the Magnaporthe oryzae conidial morphology-regulating gene COM1

<p>Abstract</p> <p>Background</p> <p>The rice blast disease caused by <it>Magnaporthe oryzae </it>is a major constraint on world rice production. The conidia produced by this fungal pathogen are the main source of disease dissemination. The morphology of conidia may be a critical factor in the spore dispersal and virulence of <it>M. oryzae </it>in the field. Deletion of a conidial morphology regulating gene encoding putative transcriptional regulator COM1 in <it>M. oryzae </it>resulted in aberrant conidial shape, reduced conidiation and attenuated virulence.</p> <p>Results</p> <p>In this study, a two-dimensional gel electrophoresis/matrix assisted laser desorption ionization- time of flight mass spectrometry (2-DE/MALDI-TOF MS) based proteomics approach was employed to identify the cellular and molecular components regulated by the COM1 protein (COM1p) that might contribute to the aberrant phenotypes in <it>M. oryzae</it>. By comparing the conidial proteomes of <it>COM1 </it>deletion mutant and its isogenic wild-type strain P131, we identified a potpourri of 31 proteins that exhibited statistically significant alterations in their abundance levels. Of these differentially regulated proteins, the abundance levels of nine proteins were elevated and twelve were reduced in the Δ<it>com1 </it>mutant. Three proteins were detected only in the Δ<it>com1 </it>conidial proteome, whereas seven proteins were apparently undetectable. The data obtained in the study suggest that the COM1p plays a key role in transcriptional reprogramming of genes implicated in melanin biosynthesis, carbon and energy metabolism, structural organization of cell, lipid metabolism, amino acid metabolism, etc. Semi-quantitative RT-PCR analysis revealed the down-regulation of genes encoding enzymes involved in melanin biosynthesis in the <it>COM1 </it>mutant.</p> <p>Conclusions</p> <p>Our results suggest that the COM1p may regulate the transcription of genes involved in various cellular processes indispensable for conidial development and appressorial penetration. These functions are likely to contribute to the effects of COM1p upon the aberrant phenotypes of <it>M. oryzae</it>.</p> <p>Reviewers</p> <p>This article is reviewed by George V. Shpakovski, Karthikeyan Sivaraman (nominated by M. Madan Babu) and Lakshminarayan M. Iyer.</p

Candidate effectors contribute to race differentiation and virulence of the lentil anthracnose pathogen Colletotrichum lentis

RT-qPCR primers used to quantify expression of Colletotrichum lentis candidate effectors in an infection time-course on lentil cultivar Eston. (XLSX 10 kb

Reverse Genetics for Functional Genomics of Phytopathogenic Fungi and Oomycetes

Sequencing of over 40 fungal and oomycete genomes has been completed. The next major challenge in modern fungal/oomycete biology is now to translate this plethora of genome sequence information into biological functions. Reverse genetics has emerged as a seminal tool for functional genomics investigations. Techniques utilized for reverse genetics like targeted gene disruption/replacement, gene silencing, insertional mutagenesis, and targeting induced local lesions in genomes will contribute greatly to the understanding of gene function of fungal and oomycete pathogens. This paper provides an overview on high-throughput reverse genetics approaches to decode fungal/oomycete genomes

Genetic and transcriptional dissection of resistance to Claviceps purpurea in the durum wheat cultivar Greenshank.

Funder: Canadian Seed Growers' Association; doi: http://dx.doi.org/10.13039/501100000071Funder: National Research Council of Canada: Canadian Wheat Improvement programFour QTL for ergot resistance (causal pathogen Claviceps purpurea) have been identified in the durum wheat cultivar Greenshank. Claviceps purpurea is a pathogen of grasses that infects flowers, replacing the seed with an ergot sclerotium. Ergot presents a significant problem to rye, barley and wheat, in particular hybrid seed production systems. In addition, there is evidence that the highly toxic alkaloids that accumulate within sclerotia can cross-contaminate otherwise healthy grain. Host resistance to C. purpurea is rare, few resistance loci having been identified. In this study, four ergot resistance loci are located on chromosomes 1B, 2A, 5A and 5B in the durum wheat cv. Greenshank. Ergot resistance was assessed through analysis of phenotypes associated with C. purpurea infection, namely the number of inoculated flowers that produced sclerotia, or resulted in ovary death but no sclerotia, the levels of honeydew produced, total sclerotia weight and average sclerotia weight and size per spike. Ergot testing was undertaken in Canada and the UK. A major effect QTL, QCp.aafc.DH-2A, was detected in both the Canadian and UK experiments and had a significant effect on honeydew production levels. QCp.aafc.DH-5B had the biggest influence on total sclerotia weight per spike. QCp.aafc.DH-1B was only detected in the Canadian experiments and QCp.aafc.DH-5A in the UK experiment. An RNASeq analysis, undertaken to identify wheat differentially expressed genes associated with different combinations of the four ergot resistance QTL, revealed a disproportionate number of DEGs locating to the QCp.aafc.DH-1B, QCp.aafc.DH-2A and QCp.aafc.DH-5B QTL intervals

Peroxisomal Alanine: Glyoxylate Aminotransferase AGT1 Is Indispensable for Appressorium Function of the Rice Blast Pathogen, Magnaporthe oryzae

The role of β-oxidation and the glyoxylate cycle in fungal pathogenesis is well documented. However, an ambiguity still remains over their interaction in peroxisomes to facilitate fungal pathogenicity and virulence. In this report, we characterize a gene encoding an alanine, glyoxylate aminotransferase 1 (AGT1) in Magnaporthe oryzae, the causative agent of rice blast disease, and demonstrate that AGT1 is required for pathogenicity of M. oryzae. Targeted deletion of AGT1 resulted in the failure of penetration via appressoria; therefore, mutants lacking the gene were unable to induce blast symptoms on the hosts rice and barley. This penetration failure may be associated with a disruption in lipid mobilization during conidial germination as turgor generation in the appressorium requires mobilization of lipid reserves from the conidium. Analysis of enhanced green fluorescent protein expression using the transcriptional and translational fusion with the AGT1 promoter and open reading frame, respectively, revealed that AGT1 expressed constitutively in all in vitro grown cell types and during in planta colonization, and localized in peroxisomes. Peroxisomal localization was further confirmed by colocalization with red fluorescent protein fused with the peroxisomal targeting signal 1. Surprisingly, conidia produced by the Δagt1 mutant were unable to form appressoria on artificial inductive surfaces, even after prolonged incubation. When supplemented with nicotinamide adenine dinucleotide (NAD+)+pyruvate, appressorium formation was restored on an artificial inductive surface. Taken together, our data indicate that AGT1-dependent pyruvate formation by transferring an amino group of alanine to glyoxylate, an intermediate of the glyoxylate cycle is required for lipid mobilization and utilization. This pyruvate can be converted to non-fermentable carbon sources, which may require reoxidation of NADH generated by the β-oxidation of fatty acids to NAD+ in peroxisomes. Therefore, it may provide a means to maintain redox homeostasis in appressoria

Genotype-Dependent Interaction of Lentil Lines with Ascochyta lentis

Ascochyta blight of lentil is a prevalent disease in many lentil producing regions and can cause major yield and grain quality losses. The most environmentally acceptable and economically profitable method of control is to develop varieties with high levels of durable resistance. Genetic studies to date suggest that ascochyta blight resistance genes (R-gene) in lentil lines CDC Robin, ILL 7537, 964a-46, and ILL 1704 are non-allelic. To understand how different R-genes manifest resistance in these genotypes and an accession of Lens ervoides, L-01-827A, with high level of resistance to ascochyta blight, cellular and molecular defense responses were compared after inoculation with the causal pathogen Ascochyta lentis. Pathogenicity testing of the resistant lines to A. lentis inoculation revealed significantly lower disease severity on CDC Robin and ILL 7537 compared to ILL 1704 and 964a-46, and no symptoms of disease were observed on L-01-827A. Histological examinations indicated that cell death triggered by the pathogen might be disrupted as a mechanism of resistance in CDC Robin. In contrast, limiting colonization of epidermal cells by A. lentis is a suggested mechanism of resistance in 964a-46. A time-series comparison of the expressions of hallmark genes in salicylic acid (SA) and jasmonic acid (JA) signal transduction pathways between CDC Robin and 964a-46 was conducted. These partially resistant genotypes differed in the timing and the magnitude of SA and JA signaling pathway activation. The SA signaling pathway was only triggered in 964a-46, whereas the JA pathway was triggered in both partially resistant genotypes CDC Robin and 964a-46. The expression of JA-associated genes was lower in 964a-46 than CDC Robin. These observations corroborate the existence of diverse ascochyta blight resistance mechanisms in lentil genotypes carrying different R-genes

Overexpression of a novel biotrophy-specific colletotrichum truncatum Effector, CtNUDIX, in hemibiotrophic fungal phytopathogens causes incompatibility with their host plants

The hemibiotrophic fungus Colletotrichum truncatum causes anthracnose disease on lentils and a few other grain legumes. It shows initial symptomless intracellular growth, where colonized host cells remain viable (biotrophy), and then switches to necrotrophic growth, killing the colonized host plant tissues. Here, we report a novel effector gene, CtNUDIX, from C. truncatum that is exclusively expressed during the late biotrophic phase (before the switch to necrotrophy) and elicits a hypersensitive response (HR)-like cell death in tobacco leaves transiently expressing the effector. CtNUDIX homologs, which contain a signal peptide and a Nudix hydrolase domain, may be unique to hemibiotrophic fungal and fungus-like plant pathogens. CtNUDIX lacking a signal peptide or a Nudix motif failed to induce cell death in tobacco. Expression of CtNUDIX:eGFP in tobacco suggested that the fusion protein might act on the host cell plasma membrane. Overexpression of CtNUDIX in C. truncatum and the rice blast pathogen, Magnaporthe oryzae, resulted in incompatibility with the hosts lentil and barley, respectively, by causing an HR-like response in infected host cells associated with the biotrophic invasive hyphae. These results suggest that C. truncatum and possibly M. oryzae elicit cell death to signal the transition from biotrophy to necrotrophy.Peer reviewed: YesNRC publication: Ye