Connectivity of Tiger (Panthera tigris) Populations in the Human-Influenced Forest Mosaic of Central India

Today, most wild tigers live in small, isolated Protected Areas within human dominated landscapes in the Indian subcontinent. Future survival of tigers depends on increasing local population size, as well as maintaining connectivity between populations. While significant conservation effort has been invested in increasing tiger population size, few initiatives have focused on landscape-level connectivity and on understanding the effect different landscape elements have on maintaining connectivity. We combined individual-based genetic and landscape ecology approaches to address this issue in six protected areas with varying tiger densities and separation in the Central Indian tiger landscape. We non-invasively sampled 55 tigers from different protected areas within this landscape. Maximum-likelihood and Bayesian genetic assignment tests indicate long-range tiger dispersal (on the order of 650 km) between protected areas. Further geo-spatial analyses revealed that tiger connectivity was affected by landscape elements such as human settlements, road density and host-population tiger density, but not by distance between populations. Our results elucidate the importance of landscape and habitat viability outside and between protected areas and provide a quantitative approach to test functionality of tiger corridors. We suggest future management strategies aim to minimize urban expansion between protected areas to maximize tiger connectivity. Achieving this goal in the context of ongoing urbanization and need to sustain current economic growth exerts enormous pressure on the remaining tiger habitats and emerges as a big challenge to conserve wild tigers in the Indian subcontinent.     

Epistatic role of base excision repair and mismatch repair pathways in mediating cisplatin cytotoxicity

Base excision repair (BER) and mismatch repair (MMR) pathways play an important role in modulating cis-Diamminedichloroplatinum (II) (cisplatin) cytotoxicity. In this article, we identified a novel mechanistic role of both BER and MMR pathways in mediating cellular responses to cisplatin treatment. Cells defective in BER or MMR display a cisplatin-resistant phenotype. Targeting both BER and MMR pathways resulted in no additional resistance to cisplatin, suggesting that BER and MMR play epistatic roles in mediating cisplatin cytotoxicity. Using a DNA Polymerase β (Polβ) variant deficient in polymerase activity (D256A), we demonstrate that MMR acts downstream of BER and is dependent on the polymerase activity of Polβ in mediating cisplatin cytotoxicity. MSH2 preferentially binds a cisplatin interstrand cross-link (ICL) DNA substrate containing a mismatch compared with a cisplatin ICL substrate without a mismatch, suggesting a novel mutagenic role of Polβ in activating MMR in response to cisplatin. Collectively, these results provide the first mechanistic model for BER and MMR functioning within the same pathway to mediate cisplatin sensitivity via non-productive ICL processing. In this model, MMR participation in non-productive cisplatin ICL processing is downstream of BER processing and dependent on Polβ misincorporation at cisplatin ICL sites, which results in persistent cisplatin ICLs and sensitivity to cisplatin.     

Albirhodobacter marinus gen. nov., sp. nov., a member of the family Rhodobacteraceae isolated from sea shore water of Visakhapatnam, India

A novel marine, Gram-negative, rod-shaped bacterium, designated strain N9^T, was isolated from a water sample of the sea shore at Visakhapatnam, Andhra Pradesh (India). Strain N9^T was found to be positive for oxidase and catalase activities. The fatty acids were found to be dominated by C_16:0, C_18:1 ω7c and summed in feature 3 (C_16:1 ω7c and/or C_16:1 ω6c). Strain N9^T was determined to contain Q-10 as the major respiratory quinone and phosphatidylethanolamine, phosphatidylglycerol, two aminophospholipids, two phospholipids and four unidentified lipids as polar lipids. The DNA G+C content of the strain N9^T was found to be 63 mol%. 16S rRNA gene sequence analysis indicated that Rhodobacter sphaeroides, Rhodobacter johrii, Pseudorhodobacter ferrugineus, Rhodobacter azotoformans, Rhodobacter ovatus and Pseudorhodobacter aquimaris were the nearest phylogenetic neighbours, with pair-wise sequence similarities of 95.43, 95.36, 94.24, 95.31, 95.60 and 94.74 %, respectively. Phylogenetic analysis showed that strain N9^T formed a distinct branch within the family Rhodobacteraceae and clustered with the clade comprising species of the genus Pseudorhodobacter, together with species of the genera Roseicitreum, Roseinatronobacter, Roseibaca and Rhodobaca. Species of the genus Pseudorhodobacter are phylogenetically close with a 16S rRNA gene sequence dissimilarity of 5.9–7.3 % (92.7–94.1 % similarity). Based on the above-mentioned phenotypic characteristics and on phylogenetic inference, strain N9^T is proposed as a representative of a new genus and a novel species of the family Rhodobacteraceae as Albirhodobacter marinus gen. nov., sp. nov. The type strain of Albirhodobacter marinus is N9 (= MTCC 11277^T = JCM 17680^T).     

Anti-platelet activity of a three-finger toxin (3FTx) from Indian monocled cobra (Naja kaouthia) venom

A low molecular weight anti-platelet peptide (6.9 kDa) has been purified from Naja kaouthia venom and was named KT-6.9. MALDI-TOF/TOF mass spectrometry analysis revealed the homology of KT-6.9 peptide sequence with many three finger toxin family members. KT-6.9 inhibited human platelet aggregation process in a dose dependent manner. It has inhibited ADP, thrombin and arachidonic acid induced platelet aggregation process in dose dependent manner, but did not inhibit collagen and ristocetin induced platelet aggregation. Strong inhibition (70%) of the ADP induced platelet aggregation by KT-6.9 suggests competition with ADP for its receptors on platelet surface. Anti-platelet activity of KT-6.9 was found to be 25 times stronger than that of anti-platelet drug clopidogrel. Binding of KT-6.9 to platelet surface was confirmed by surface plasma resonance analysis using BIAcore X100. Binding was also observed by a modified sandwich ELISA method using anti-KT-6.9 antibodies. KT-6.9 is probably the first 3FTx from Indian monocled cobra venom reported as a platelet aggregation inhibitor.