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Browsing by Author "Sahu, Pranav P."

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    Geminiviruses and plant hosts: a closer examination of the molecular arms race
    (MDPI AG, 2017) Ramesh, Shunmugiah V.; Sahu, Pranav P.; Prasad, Manoj; Praveen, Shelly; Pappu, Hanu R.
    Geminiviruses are plant-infecting viruses characterized by a single-stranded DNA (ssDNA) genome. Geminivirus-derived proteins are multifunctional and effective regulators in modulating the host cellular processes resulting in successful infection. Virus-host interactions result in changes in host gene expression patterns, reprogram plant signaling controls, disrupt central cellular metabolic pathways, impair plant's defense system, and effectively evade RNA silencing response leading to host susceptibility. This review summarizes what is known about the cellular processes in the continuing tug of war between geminiviruses and their plant hosts at the molecular level. In addition, implications for engineered resistance to geminivirus infection in the context of a greater understanding of the molecular processes are also discussed. Finally, the prospect of employing geminivirus-based vectors in plant genome engineering and the emergence of powerful genome editing tools to confer geminivirus resistance are highlighted to complete the perspective on geminivirus-plant molecular interactions.
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    Role of host transcription factors in modulating defense response during plant-virus interaction
    (Caister Academic Press, 2018) Pandey, Saurabh; Sahu, Pranav P.; Kulshreshtha, Ritika; Prasad, Manoj
    Plants are vulnerable to several environmental stresses either biotic or abiotic due to their sessile nature. Consequently, they assimilate various responses to counter and acclimate in ever-changing environments. One of the fascinating response is transcriptional reprogramming of cell leading to defense or stress adaptation. It is imperative to recognize transcription factors which are associated with plant defense responses against biotic agents such as viruses. Members of families belonging to WRKY family of transcription factor, myeloblastosis-related proteins (MYB), basic leucine zipper (bZIP), Apetela2/ethylene-responsive element binding (AP2/ERF), and NAC transcription factors have been shown to be associated with innumerable defense response against plant virus. These TF family members interact directly or indirectly to modulate defense response by activation or repression of downstream signaling pathways. Hence the gaining insight between plant virus and TFs interplay and deciphering the alterations in defense pathway are the prerequisite to engineer crops for tolerance to biotic stresses. In this chapter, we have attempted to summarize the explicit role of TFs in modulating the expression of defense genes during plant-virus interaction.
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    Surfacing the role of epigenetics in host-virus interaction
    (Caister Academic Press, 2018) Sharma, Namisha; Sahu, Pranav P.; Kulshreshtha, Ritika; Prasad, Manoj
    Epigenetics is a mechanism which determines the phenotype of an organism by causing heritable (during cell division) but simultaneously reversible alterations/variations in gene expression. It is not related to alterations in the DNA sequence of the genotype. Geminiviruses are the most devastating plant viruses since they cause significant yield losses in world agriculture. The plant defense initiated against these DNA viruses is of special interest, specifically in regard to the role of epigenetic mechanism played in control of virus spread. These heritable and covalent modifications of DNA and histone in virus genome are mainly related to suppression of gene transcription, despite the differences between viruses, the role of epigenetics seems to be reasonably comparable. However, several key questions remain unanswered concerning the basic mechanism behind the epigenetic regulation of viruses via plant defense system. This book chapter specifically summarizes the recent advances on role of epigenetics in virus genome modification leading to silencing of viral genes and plant tolerance/resistance.

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