Veerendra Kumar Sharma

Magnetocaloric effect in Heusler alloys Ni50Mn34In16 and Ni50Mn34Sn16

We present results of detailed ac susceptibility, magnetization and specific heat measurements in Heusler alloys Ni50Mn34In16 and Ni50Mn34Sn16. These alloys undergo a paramagnetic to ferromagnetic transition around 305 K, which is followed by a martensitic transition in the temperature regime around 220 K. Inside the martensite phase both the alloys show signatures of field-induced transition from martensite to austenite phase. Both field- and temperature-induced martensite–austenite transitions are relatively sharp in Ni50Mn34In16. We estimate the isothermal magnetic entropy change and adiabatic temperature change across the various phase transitions in these alloys and investigate the possible influence of these transitions on the estimated magnetocaloric effect. The sharp martensitic transition in Ni50Mn34In16 gives rise to a comparatively large inverse magnetocaloric effect across this transition. On the other hand the magnitudes of the conventional magnetocaloric effect associated with the paramagnetic to ferromagnetic transition are quite comparable in these alloys.

The effect of substitution of Mn by Fe and Cr on the martensitic transition in the Ni50Mn34In16 alloy

The potential shape memory alloy Ni(50)Mn(34)In(16) is studied with partial substitution of Mn with Fe and Cr to investigate the effect of such substitution on the martensitic transition in the Ni-Mn-In alloy system. The results of ac susceptibility, magnetization and electrical resistivity measurements show that while the substitution with Cr increases the martensitic transition temperature, the substitution with Fe decreases it. Possible reasons for this shift in martensitic transition are discussed. Evidence of kinetic arrest of the austenite to martensite phase transition in the Fe substituted alloys is also presented. Unlike the kinetic arrest of the austenite to martensite phase transition in the parent Ni(50)Mn(34)In(16) alloy which takes place in the presence of high external magnetic field, the kinetic arrest of the austenite to martensite phase transition in the Fe doped alloy occurs even in zero magnetic field. The Cr substituted alloys, on the other hand, show no signature of kinetic arrest of this phase transition.

A geminivirus betasatellite damages the structural and functional integrity of chloroplasts leading to symptom formation and inhibition of photosynthesis

Highlight A satellite DNA-encoded protein (βC1) is localized in the chloroplast. The intercellular events associated with βC1-induced photosynthetic inhibition and vein clearing symptom formation are discussed.

A novel recombinant tomato-infecting begomovirus capable of transcomplementing heterologous DNA-B components

The genome of a tomato-infecting begomovirus from Ranchi, India, was cloned, sequenced and analysed. The viral genome shared 88.3% sequence identity with an isolate belonging to the species Tobacco curly shoot virus (TbCSV), and this virus should therefore be considered a member of a new species, tentatively named Tomato leaf curl Ranchi virus (ToLCRnV). The DNA-β molecule, which had 74.5% sequence identity with tomato leaf curl Bangladesh betasatellite (ToLCBDB), is named tomato leaf curl Ranchi betasatellite (ToLCRnB). Phylogenetic analysis revealed that ToLCRnV is related to tomato leaf curl Bangladesh virus (ToLCBDV), tobacco curly shoot virus (TbCSV) and tomato leaf curl Gujarat virus (ToLCGV). An infectivity study with ToLCRnV established the monopartite nature of the viral genome, whereas inoculation with ToLCRnB resulted in increased symptom severity. ToLCRnV could transreplicate DNA-B of tomato leaf curl Gujarat virus (ToLCGV) and tomato leaf curl New Delhi virus (ToLCNDV), both in N. benthamiana and tomato, although DNA-B accumulation of was less than with the wild-type combinations. ToLCRnB could be efficiently replicated by DNA-A of both ToLCNDV and ToLCGV. A leaf disk assay suggests that DNA-A could transreplicate the homologous DNA-B and DNA-β more efficiently than the heterologous one.

Identification of siRNA generating hot spots in multiple viral suppressors to generate broad-spectrum antiviral resistance in plants

Viruses are one of the most devastating plant pathogens causing severe economic losses worldwide. RNA silencing is a robust technology to knock down the expression of specific genes. This mechanism can be exploited to generate virus resistant plants through expression of the viral derived sequences. Viruses in turn have evolved to encode suppressors of RNA silencing to combat host defense. Mixed infection of plants is of common occurrence in nature and simultaneous targeting of suppressor(s) of multiple viruses offers an effective strategy. In this study, we have in silico designed siRNAs against suppressors of the two most devastating viruses of tomato, leaf curl causing tomato begomoviruses and Cucumber mosaic virus. Three different siRNA prediction programs were used to evaluate siRNAs generating capability of each sequence and common putative candidate siRNAs were selected fulfilling the stringent parameters. Our results indicated that in the case of each suppressor a particular region of 100–150 base pairs could be source of potent siRNAs referred as hotspots. Expression of these viral hot spots as a single construct in the plants would facilitate development of transgenic plants with a high degree of broad spectrum resistance against multiple viruses.

An Overview of Antiviral RNA Silencing in Plant: Biogenesis, Host-Virus Interaction and Potential Applications

Small RNA molecules play a crucial regulatory role in maintaining genome stability as well as developmental regulations through a set of complex and partially overlapping pathways in a wide range of eukaryotic organisms. Active in both cytoplasm and nucleus, RNA interference regulates eukaryotic gene expression through transcriptional repression by epigenetic modification and interaction with transcription machinery. Small interfering RNAs (siRNAs/miRNAs) of 21–24 nucleotides constitute the innate defence arm against a variety of pathogens, especially viruses. Plant viruses with either DNA or RNA genomes are subjected to small RNA-directed RNA degradation. Additionally, DNA viruses are subjected to another line of defence through ‘RNA-directed DNA methylations’ (RdDM). On the other hand, viral-encoded proteins, called silencing suppressors (VSRs), are known to counter the defence machinery, and therefore the virus can evade the host surveillance system. Some plant viruses additionally adopt certain strategies like acquiring silencing resistant structures (some RNA virus) to evade the RNA silencing machinery and thereby shaping the viral as well as the host genome. Recently, it has been reported that particular viral proteins and viral siRNAs contribute directly to pathogenicity by interacting with certain host proteins or RNAs. Transcriptional regulation of host gene by small RNA of viral origin plays important role in pathogenesis and symptom development. Small regulatory RNAs of cellular rather than pathogen origin have also been found to play a broad role in improving the basal defence in the case of plant–virus interaction. This chapter provides key insights into the complex intricate machinery of diverse RNA silencing mechanisms, describes various evolutionary diverse strategies of viral silencing suppressors at various steps, offers a broader view of host recovery following virus infection and finally suggests the possible applications of RNA silencing to generate virus resistant plants.