Pallob Kundu

Bio: Pallob Kundu is an academic researcher from Bose Institute. The author has contributed to research in topics: Promoter & Gene. The author has an hindex of 16, co-authored 27 publications receiving 720 citations. Previous affiliations of Pallob Kundu include University of California, Los Angeles & University of California.

Method to Study Dynamics of Membrane-Bound Plant Transcription Factors During Biotic Interactions in Tomato.

Abstract: Sequestration of a transcription factor in a cellular membrane and releasing it on demand is an additional layer of gene regulation that is considered a rapid mode to reprogram a gene expression cascade when a plasma membrane stress signal is perceived. Better understanding of the dynamic exchange of membrane-bound transcription factors (MTFs) during biotic stress requires the development of a simple, efficient, and quick assay system. Here we report an Agrobacterium-based transient transformation method to assay the localization of fluorescent protein-tagged MTFs in tomato leaf epidermal peels that are subsequently infected with a pathogenic fungus. Essentially, our method mimics natural infection and facilitates the realistic monitoring of MTF movement during activation of a signaling event.

Disruption of tomato TGS machinery by ToLCNDV causes reprogramming of vascular tissue-specific TORNADO1 gene expression

Abstract: Vascular development-related TRN1 transcription is suppressed by cytosine methylation in fully developed leaves of tomato. ToLCNDV infection disrupts methylation machinery and reactivates TRN1 expression - likely causing abnormal leaf growth pattern. Leaf curl disease of tomato caused by tomato leaf curl New Delhi virus (ToLCNDV) inflicts huge economical loss. Disease symptoms resemble leaf developmental defects including abnormal vein architecture. Leaf vein patterning-related TORNADO1 gene’s (SlTRN1) transcript level is augmented in virus-infected leaves. To elucidate the molecular mechanism of the upregulation of SlTRN1 in vivo, we have deployed SlTRN1 promoter-reporter transgenic tomato plants and investigated the gene’s dynamic expression pattern in leaf growth stages and infection. Expression of the gene was delimited in the vascular tissues and suppressed in fully developed leaves. WRKY16 transcription factor readily activated SlTRN1 promoter in varied sized leaves and upon virus infection, while silencing of WRKY16 gene resulted in dampened promoter activity. Methylation-sensitive PCR analyses confirmed the accumulation of CHH methylation at multiple locations in the SlTRN1 promoter in older leaves. However, ToLCNDV infection reverses the methylation status and restores expression level in the leaf vascular bundle. The virus dampens the level of key maintenance and de novo DNA methyltransferases SlDRM5, SlMET1, SlCMT2 with concomitant augmentation of two DNA demethylases, SlDML1 and SlDML2 levels in SlTRN1 promoter-reporter transgenics. Transient overexpression of SlDML2 mimics the virus-induced hypomethylation state of the SlTRN1 promoter in mature leaves, while silencing of SlDML2 lessens promoter activity. Furthermore, in line with the previous studies, we confirm the crucial role of viral suppressors of RNA silencing AC2 and AC4 proteins in promoting DNA demethylation and directing it to restore activated transcription of SlTRN1. Unusually elevated expression of SlTRN1 may negatively impact normal growth of leaves.

Foot-and-Mouth Disease

Abstract: Foot-and-mouth disease (FMD) is a highly contagious disease of cloven-hoofed animals. The disease was initially described in the 16th century and was the first animal pathogen identified as a virus. Recent FMD outbreaks in developed countries and their significant economic impact have increased the concern of governments worldwide. This review describes the reemergence of FMD in developed countries that had been disease free for many years and the effect that this has had on disease control strategies. The etiologic agent, FMD virus (FMDV), a member of the Picornaviridae family, is examined in detail at the genetic, structural, and biochemical levels and in terms of its antigenic diversity. The virus replication cycle, including virus-receptor interactions as well as unique aspects of virus translation and shutoff of host macromolecular synthesis, is discussed. This information has been the basis for the development of improved protocols to rapidly identify disease outbreaks, to differentiate vaccinated from infected animals, and to begin to identify and test novel vaccine candidates. Furthermore, this knowledge, coupled with the ability to manipulate FMDV genomes at the molecular level, has provided the framework for examination of disease pathogenesis and the development of a more complete understanding of the virus and host factors involved.

Antimicrobial Peptides: Classification, Design, Application and Research Progress in Multiple Fields

Abstract: Antimicrobial peptides (AMPs) are a class of small peptides that widely exist in nature and they are an important part of the innate immune system of different organisms. AMPs have a wide range of inhibitory effects against bacteria, fungi, parasites and viruses. The emergence of antibiotic-resistant microorganisms and the increasing of concerns about the use of antibiotics resulted in the development of AMPs, which have a good application prospect in medicine, food, animal husbandry, agriculture and aquaculture. This review introduces the progress of research on AMPs comprehensively and systematically, including their classification, mechanism of action, design methods, environmental factors affecting their activity, application status, prospects in various fields and problems to be solved. The research progress on antivirus peptides, especially anti-coronavirus (COVID-19) peptides, has been introduced given the COVID-19 pandemic worldwide in 2020.

Severe acute respiratory syndrome coronavirus nsp1 protein suppresses host gene expression by promoting host mRNA degradation.

Abstract: Severe acute respiratory syndrome (SARS) coronavirus (SCoV) causes a recently emerged human disease associated with pneumonia. The 5′ end two-thirds of the single-stranded positive-sense viral genomic RNA, gene 1, encodes 16 mature proteins. Expression of nsp1, the most N-terminal gene 1 protein, prevented Sendai virus-induced endogenous IFN-β mRNA accumulation without inhibiting dimerization of IFN regulatory factor 3, a protein that is essential for activation of the IFN-β promoter. Furthermore, nsp1 expression promoted degradation of expressed RNA transcripts and host endogenous mRNAs, leading to a strong host protein synthesis inhibition. SCoV replication also promoted degradation of expressed RNA transcripts and host mRNAs, suggesting that nsp1 exerted its mRNA destabilization function in infected cells. In contrast to nsp1-induced mRNA destablization, no degradation of the 28S and 18S rRNAs occurred in either nsp1-expressing cells or SCoV-infected cells. These data suggested that, in infected cells, nsp1 promotes host mRNA degradation and thereby suppresses host gene expression, including proteins involved in host innate immune functions. SCoV nsp1-mediated promotion of host mRNA degradation may play an important role in SCoV pathogenesis.

Severe Acute Respiratory Syndrome Coronavirus nsp1 Suppresses Host Gene Expression, Including That of Type I Interferon, in Infected Cells

Abstract: The severe acute respiratory syndrome coronavirus (SARS-CoV) nsp1 protein has unique biological functions that have not been described in the viral proteins of any RNA viruses; expressed SARS-CoV nsp1 protein has been found to suppress host gene expression by promoting host mRNA degradation and inhibiting translation. We generated an nsp1 mutant (nsp1-mt) that neither promoted host mRNA degradation nor suppressed host protein synthesis in expressing cells. Both a SARS-CoV mutant virus, encoding the nsp1-mt protein (SARS-CoV-mt), and a wild-type virus (SARS-CoV-WT) replicated efficiently and exhibited similar one-step growth kinetics in susceptible cells. Both viruses accumulated similar amounts of virus-specific mRNAs and nsp1 protein in infected cells, whereas the amounts of endogenous host mRNAs were clearly higher in SARS-CoV-mt-infected cells than in SARS-CoV-WT-infected cells, in both the presence and absence of actinomycin D. Further, SARS-CoV-WT replication strongly inhibited host protein synthesis, whereas host protein synthesis inhibition in SARS-CoV-mt-infected cells was not as efficient as in SARS-CoV-WT-infected cells. These data revealed that nsp1 indeed promoted host mRNA degradation and contributed to host protein translation inhibition in infected cells. Notably, SARS-CoV-mt infection, but not SARS-CoV-WT infection, induced high levels of beta interferon (IFN) mRNA accumulation and high titers of type I IFN production. These data demonstrated that SARS-CoV nsp1 suppressed host innate immune functions, including type I IFN expression, in infected cells and suggested that SARS-CoV nsp1 most probably plays a critical role in SARS-CoV virulence.