Literature based species occurrence data of birds of northeast India

The northeast region of India is one of the world's most significant biodiversity hotspots. One of the richest bird areas in India, it is an important route for migratory birds and home to many endemic bird species. This paper describes a literature-based dataset of species occurrences of birds of northeast India. The occurrence records documented in the dataset are distributed across eleven states of India, viz.: Arunachal Pradesh, Assam, Bihar, Manipur, Meghalaya, Mizoram, Nagaland, Sikkim, Tripura, Uttar Pradesh and West Bengal. The geospatial scope of the dataset represents 24 to 29 degree North latitude and 78 to 94 degree East longitude, and it comprises over 2400 occurrence records. These records have been collated from scholarly literature published between1915 and 2008, especially from the Journal of the Bombay Natural History Society (JBNHS). The temporal scale of the dataset represents bird observations recorded between 1909 and 2007. The dataset has been developed by employing MS Excel. The key elements in the database are scientific name, taxonomic classification, temporal and geospatial details including geo-coordinate precision, data collector, basis of record and primary source of the data record. The temporal and geospatial quality of more than 50% of the data records has been enhanced retrospectively. Where possible, data records are annotated with geospatial coordinate precision to the nearest minute. This dataset is being constantly updated with the addition of new data records, and quality enhancement of documented occurrences. The dataset can be used in species distribution and niche modeling studies. It is planned to expand the scope of the dataset to collate bird species occurrences across the Indian peninsula.     

Temperature-dependent STIM1 activation induces Ca²+ influx and modulates gene expression

Intracellular Ca(2+) is essential for diverse cellular functions. Ca(2+) entry into many cell types including immune cells is triggered by depleting endoplasmic reticulum (ER) Ca(2+), a process termed store-operated Ca(2+) entry (SOCE). STIM1 is an ER Ca(2+) sensor. Upon Ca(2+) store depletion, STIM1 clusters at ER-plasma membrane junctions where it interacts with and gates Ca(2+)-permeable Orai1 ion channels. Here we show that STIM1 is also activated by temperature. Heating cells caused clustering of STIM1 at temperatures above 35 °C without depleting Ca(2+) stores and led to Orai1-mediated Ca(2+) influx as a heat off-response (response after cooling). Notably, the functional coupling of STIM1 and Orai1 is prevented at high temperatures, potentially explaining the heat off-response. Additionally, physiologically relevant temperature shifts modulate STIM1-dependent gene expression in Jurkat T cells. Therefore, temperature is an important regulator of STIM1 function.     

Correlated behavior implicates stromules in increasing the interactive surface between plastids and ER tubules

Stromules are extended by plastids but the underlying basis for their extension and retraction had not been understood until recently. Our live-imaging aided observations on coincident plastid stromule branching and ER tubule dynamics open out new areas of investigation relating to these rapid subcellular interactions. This addendum provides a testable hypothesis on the formation of stromules, which argues against the need for new membrane incorporation and suggests that stromal extensions might result from a remodeling of the plastid envelope membrane in an ER aided manner.Key words: stromules, plastids, endoplasmic reticulum, fluorescent proteins, subcellular interactions, FNR-EGFP, RFP-ERThe extension and retraction of stromules (stroma-filled tubules) from both chlorophyll containing and achlorophyllous plastids is well established for diverse plant species.¹ Many different conditions such as increased subcellular redox stress,² symbiotic interactions,^3–5 elevated temperatures,⁶ viral infection⁷ and alterations in plastid size and density^8,9 have been associated with stromule formation. Stromules extended from different plastids have been observed as forming connecting bridges^10–13 through which an exchange of proteins has been demonstrated.^{10,11,14–16} The latter observations strongly suggested stromules as transient communication channels between plastids for exchanging metabolites.^10,11 The connectivity of plastids via stromules also led to the suggestion that plant cells might contain a plastidom, defined as a well-connected plastid-compartment.¹² However, as pointed out by Netasan and co-workers¹⁷ most stromules do not appear to interconnect plastids and thus the movement of macromolecules between plastids might not be their sole function. In concurrence with this viewpoint the observations of Gunning¹⁸ and Lütz and Engel¹⁹ suggest that stromules have a role in increasing plastid interactions with mitochondria and peroxisomes. Thus a more generalized and acceptable statement is that stromules serve to increase the plastid stromal surface area that is exposed to the subcellular environment.Notably, the largest membrane surface area within a cell is provided by the endoplasmic reticulum (ER). Transmission electron micrographs often suggest a close proximity between plastids and the ER^20,21 and the presence of a chloroplast envelope associated-ER has been demonstrated.²² However, studies aimed at uncovering possible dynamic interactions between stromules and the ER in living plant cells had not been carried out. Our recent work²³ investigated this possible relationship by simultaneously visualizing stromules (labeled using a ferredoxin NADP(H) oxidoreductase (FNR) transit peptide fused to enhanced GFP; hereafter referred to as FNR-EGFP) and the ER (highlighted using a chimeric red fluorescent protein (RFP) carrying a basic chitinase signal sequence and an ER retention sequence; referred to as RFP-ER). Our observations clearly identified the ER as providing the nearest set of membranes with which the plastid envelope can interact. The observations are most pertinent for the narrow cortical sleeve where the relatively large sized plastids (including chloroplasts) are pressed against the cell boundary (plasma membrane and comparatively rigid cell wall) on one side and a turgid vacuole on the inner side. This space is also traversed by the cortical ER mesh created by constantly reorganizing ER-tubules. As shown in Figure 1A the side of a plastid pressed against the plasma membrane is surrounded by a loose mesh of ER tubules while the side pressed close to the vacuolar membrane (Fig. 1B) is free of the ER cradle. The cortically located plastids display strong behavioral correlations between their stromules and the neighboring ER tubules (Fig. 1C–E). Notably stromules form triangular junctions that appear very similar to the 3-way junctions displayed by the cortical ER. The three-way junctions of the ER are cisternal locations from which tubules are extended to create ER polygons. Stromule branches are extended from the stromal triangles in a very similar manner along comparable angles. Interestingly the extension and retraction of stromules and their branches occurs in tandem with contiguous ER tubules. These observations on the coincident behavior of the two organelles indicate that stromule branching and dynamic behavior might rely upon the creation of multiple membrane contact sites (MCSs) with the ER. The MCSs could aid in stretching stromules along ER tubules while loss of contact between the two membranes could cause rapid stromule retraction. While the possibility of identifying MCSs on the stromule envelope is being explored further by us our initial observations evoke a long-standing but very relevant question. Where does the membrane for forming stromules come from?Open in a separate windowFigure 1Confocal laser scanning microscopy based imaging of living Nicotiana benthamiana cells co-expressing FNR-EGFP (labels stromules) and RFP-ER (labels ER), 3D isosurface rendering and a model based on the observations. (A) 3D iso-surface rendering of a chloroplast facing the plasma membrane side shows the plastid situated in a loose cradle of ER tubules. (B) The 3D rendered chloroplast ER reconstruction seen in (A) observed from the vacuolar side after rotation by 180° shows the chloroplast appears smooth and free of the ER mesh. (C–E) Sequential frames from a time-lapse movie depict a FNR-EGFP labeled stromule undergoing a branching event. Note that in (C) the stromule extending along an ER channel with possible contacts at several points along the stromule length. (D) depicts a stromal triangle (arrowhead) that forms a branch initial. (E) depicts a branched stromule with the branches aligned with the ER (size bar = 5 µm). (F) A plastid exhibiting a short, wide stroma-filled area after stromule retraction has occured. (G) The same plastid shown in (F) without the FNR-EGFP labeled stroma (arrowhead) provides an appreciation of the “mobile jacket” created by the stromal contents around the chlorophyll containing thylakoids (size bar = 5 µm). (H and I) A diagrammatic depiction based on our observations and pertinent literature. (H) The narrow cortical region between the vacuolar membrane and the cell boundary is shared by large plastids and a dynamic ER. A depiction of the loose stroma filled jacket (arrowhead) of a plastid along with contiguous ER. Note the relative positions of the vacuolar membrane and the plasma membrane. The plastid size cannot increase isotropically within the narrow confines of the cortex and thus stromule formation along ER tubules is favored (Arrow pointing direction of stromule extension along the ER). (I) Multiple contact sites might be created between the extending stromule and the neighboring ER tubules. The diagrammatic depiction emphasizes the remodeling of the loose plastid jacket for stromule extension along ER. The schematic does not depict the strong possibility that both organelles might share an F-actin based mechanism for their extension.Stromule extension visibly enlarges the area occupied by the stromal contents of a plastid. The general conclusion of stromules increasing the plastid surface is clearly validated. Indeed Hanson and coworkers¹ calculated that for a model plastid of 3 µm diameter extending a 0.2 µm diameter and 10 µm long stromule the stromule represents about 20% of the overall plastid envelope surface area. A point that remains unclear is whether stromule extension involves a net increase in plastidic membrane or merely involves a remodeling of the existing membrane into an elongated shape. In the first scenario stromule formation would involve the creation of fresh membrane vesicles and their incorporation into an existing bi-layered plastid coat. This would be followed by their dispersal into inner and outer plastid envelopes along with complete complements of protein import and export machinery. Currently there is no experimental evidence to support this scenario. Moreover, this viewpoint does not consider observations of stromule retraction at all. If new membranes have been added during stromule extension then what happens to them during the retraction stage? Further, live imaging clearly shows that the time involved in sporadic stromule extension, branching and retraction is in the order of seconds to minutes. Such short periods do not favor the viewpoint involving creation of new membrane and its incorporation into stromules.Interestingly, observations of plastids in living cells often suggest that they have a rather wobbly form than a tight compact shape. The unstable form suggests the presence of relaxed membranes enveloping the main plastid body (Fig. 1F and G). These loose fitting membranes have been described as a “mobile jacket”^1,24 whose presence and irregular protrusions can be clearly distinguished from long stromules using a shape index.⁶ Hanson and co-workers¹ speculated that the “mobile jacket” might be stretched out and could thus provide the extra membrane needed for stromule formation. The notion is supported by the work of Gunning, which shows stromules retracting into short amorphous protrusions.¹⁸ Our observations of short protrusions or “beaks”²³ being created sporadically on a relatively regular-appearing plastid surface support these ideas. According to our observations one or two of the beaks might develop into long stromules that would be extended along neighboring ER tubules (Fig. 1H and I).Moreover, in vitro experiments on sucrose filled liposomes and giant vesicles^25,26 are particularly interesting in this context. Plasmolytic shrinkage of the sucrose filled vesicles creates states in which excess membrane surrounds a small volume. Over time the membrane exhibits small protrusions that are very similar in shape to the protrusions formed by plastid. Taken together the above-mentioned observations support behavior that might be expected upon a reshaping of already existing membranes. Notably the membrane-remodeling scenario for the formation of a stromule does not involve an increase in the net membrane of a plastid but it does achieve an increase in the surface area over which plastid stromal contents can interact with their surroundings. The viewpoint is also able to explain stromule elasticity that is suggested by their rapid extension and retraction.The new observations and ensuing discussion suggesting stromules being formed by stretching of the plastid envelope and identifying the ER as an interactive membrane partner in the process lay down the foundation for a number of other questions. These include investigations relating to the role of stromules in metabolite import and export between the two organelles, understanding the relationship between stromule and the ER behavior in relation to the underlying actin cytoskeleton as well as assessing the specificity of myosin motors that might be involved in these dynamic processes.     

Applied osmotic loading for promoting development of engineered cartilage

This study investigated the potential use of static osmotic loading as a cartilage tissue engineering strategy for growing clinically relevant grafts from either synovium-derived stem cells (SDSCs) or chondrocytes. Bovine SDSCs and chondrocytes were individually encapsulated in 2% w/v agarose and divided into chondrogenic media of osmolarities 300 (hypotonic), 330 (isotonic), and 400 (hypertonic, physiologic) mOsM for up to 7 weeks. The application of hypertonic media to constructs comprised of SDSCs or chondrocytes led to increased mechanical properties as compared to hypotonic (300 mOsM) or isotonic (330 mOsM) media (p<0.05). Constant exposure of SDSC-seeded constructs to 400 mOsM media from day 0 to day 49 yielded a Young's modulus of 513±89 kPa and GAG content of 7.39±0.52%ww on day 49, well within the range of values of native, immature bovine cartilage. Primary chondrocyte-seeded constructs achieved almost as high a Young's modulus, reaching 487±187 kPa and 6.77±0.54%ww (GAG) for the 400 mOsM condition (day 42). These findings suggest hypertonic loading as a straightforward strategy for 3D cultivation with significant benefits for cartilage tissue engineering strategies. In an effort to understand potential mechanisms responsible for the observed response, cell volume measurements in response to varying osmotic conditions were evaluated in relation to the Boyle–van't Hoff (BVH) law. Results confirmed that chondrocytes behave as perfect osmometers; however SDSCs deviated from the BVH relation.     

Protein Kinase A and Phosphodiesterase-4D3 Binding to Coding Polymorphisms of Cardiac Muscle Anchoring Protein (mAKAP)

Protein kinase A (PKA) substrate phosphorylation is facilitated through its co-localization with its signaling partner by A-kinase anchoring proteins (AKAPs). mAKAP (muscle-selective AKAP) localizes PKA and its substrates such as phosphodiesterase-4D3 (PDE4D3), ryanodine receptor, and protein phosphatase 2A (PP2A) to the sarcoplasmic reticulum and perinuclear space. The genetic role of mAKAP, in modulating PKA/PDE4D3 molecular signaling during cardiac diseases, remains unclear. The purpose of this study was to examine the effects of naturally occurring mutations in human mAKAP on PKA and PDE4D3 signaling. We have recently identified potentially important human mAKAP coding non-synonymous polymorphisms located within or near key protein binding sites critical to β-adrenergic receptor signaling. Three mutations (P1400S, S2195F, and L717V) were cloned and transfected into a mammalian cell line for the purpose of comparing whether those substitutions disrupt mAKAP binding to PKA or PDE4D3. Immunoprecipitation study of mAKAP-P1400S, a mutation located in the mAKAP-PDE4D3 binding site, displayed a significant reduction in binding to PDE4D3, with no significant changes in PKA binding or PKA activity. Conversely, mAKAP-S2195F, a mutation located in mAKAP-PP2A binding site, showed significant increase in both binding propensity to PKA and PKA activity. Additionally, mAKAP-L717V, a mutation flanking the mAKAP-spectrin repeat domain, exhibited a significant increase in PKA binding compared to wild type, but there was no change in PKA activity. We also demonstrate specific binding of wild-type mAKAP to PDE4D3. Binding results were demonstrated using immunoprecipitation and confirmed with surface plasmon resonance (Biacore-2000); functional results were demonstrated using activity assays, Ca^2 + measurements, and Western blot. Comparative analysis of the binding responses of mutations to mAKAP could provide important information about how these mutations modulate signaling.     

Preparation and evaluation of a 99mTcN–PNP complex of sanazole analogue for detecting tumor hypoxia

A sanazole derivative, having a favorable single electron reduction potential (SERP) value compared to that of misonidazole, was synthesized and radiolabeled with [^99mTcN(PNP)] precursor to evaluate its potential as a hypoxia imaging agent. The complex, which was lipophilic, could be prepared in good yields and challenging studies with cysteine showed stability of the complex against trans-chelation. However, despite being lipophilic as well as possessing favorable SERP value, biodistribution studies of this complex in fibrosarcoma tumor bearing Swiss mice showed low uptake in tumor. This observation is possibly attributed to fast clearance of the complex from blood, whereby the complex spends insufficient time in tumor to get reduced and trapped. Though uptake in tumor was low, slow clearance of activity from tumor suggests reduction and trapping of the complex in hypoxic cells. The present ^99mTc-complex demonstrated acceptable values of tumor to blood (TBR) and tumor to muscle (TMR) ratios. However, low uptake in tumor which may not be indicative of the actual hypoxic status of the tumor, limit the utility of the complex to detect tumor hypoxia.     

The differential stress response of adapted chromite mine isolates Bacillus subtilis and Escherichia coli and its impact on bioremediation potential

In the current study, indigenous bacterial isolates Bacillus subtilis VITSUKMW1 and Escherichia coli VITSUKMW3 from a chromite mine were adapted to 100 mg L^?1 of Cr(VI). The phase contrast and scanning electron microscopic images showed increase in the length of adapted E. coli cells and chain formation in case of adapted B. subtilis. The presence of chromium on the surface of the bacteria was confirmed by energy dispersive X-ray spectroscopy (EDX), which was also supported by the conspicuous Cr–O peaks in FTIR spectra. The transmission electron microscopic (TEM) images of adapted E. coli and B. subtilis showed the presence of intact cells with Cr accumulated inside the bacteria. The TEM–EDX confirmed the internalization of Cr(VI) in the adapted cells. The specific growth rate and Cr(VI) reduction capacity was significantly higher in adapted B. subtilis compared to that of adapted E. coli. To study the possible role of Cr(VI) toxicity affecting the Cr(VI) reduction capacity, the definite assays for the released reactive oxygen species (ROS) and ROS scavenging enzymes (SOD and GSH) were carried out. The decreased ROS production as well as SOD and GSH release observed in adapted B. subtilis compared to the adapted E. coli corroborated well with its higher specific growth rate and increased Cr(VI) reduction capacity.     

Role of protein kinase N2 (PKN2) in cigarette smoke-mediated oncogenic transformation of oral cells

Smoking is the leading cause of preventable death worldwide. Though cigarette smoke is an established cause of head and neck cancer (including oral cancer), molecular alterations associated with chronic cigarette smoke exposure are poorly studied. To understand the signaling alterations induced by chronic exposure to cigarette smoke, we developed a cell line model by exposing normal oral keratinocytes to cigarette smoke for a period of 12 months. Chronic exposure to cigarette smoke resulted in increased cellular proliferation and invasive ability of oral keratinocytes. Proteomic and phosphoproteomic analyses showed dysregulation of several proteins involved in cellular movement and cytoskeletal reorganization in smoke exposed cells. We observed overexpression and hyperphosphorylation of protein kinase N2 (PKN2) in smoke exposed cells as well as in a panel of head and neck cancer cell lines established from smokers. Silencing of PKN2 resulted in decreased colony formation, invasion and migration in both smoke exposed cells and head and neck cancer cell lines. Our results indicate that PKN2 plays an important role in oncogenic transformation of oral keratinocytes in response to cigarette smoke. The current study provides evidence that PKN2 can act as a potential therapeutic target in head and neck squamous cell carcinoma, especially in patients with a history of smoking.     

Enhanced expression of ginsenoside biosynthetic genes and in vitro ginsenoside production in elicited <Emphasis Type="Italic">Panax sikkimensis</Emphasis> (Ban) cell suspensions

Dual metabolite, i.e., ginsenoside and anthocyanin, co-accumulating cell suspensions of Panax sikkimensis were subjected to elicitation with culture filtrates of Serratia marcescens (SD 21), Bacillus subtilis (FL11), Trichoderma atroviridae (TA), and T. harzianum (TH) at 1.25% and 2.5% v/v for 1- and 3-week duration. The fungal-derived elicitors (TA and TH) did not significantly affect biomass accumulation; however, bacterial elicitors (SD 21 and FL11), especially SD 21, led to comparable loss in biomass growth. In terms of ginsenoside content, differential responses were observed. A maximum of 3.2-fold increase (222.2 mg/L) in total ginsenoside content was observed with the use of 2.5% v/v TH culture filtrate for 1 week. Similar ginsenoside accumulation was observed with the use of 1-week treatment with 2.5% v/v SD 21 culture filtrate (189.3 mg/L) with a 10-fold increase in intracellular Rg2 biosynthesis (31 mg/L). Real-time PCR analysis of key ginsenoside biosynthesis genes, i.e., FPS, SQS, DDS, PPDS, and PPTS, revealed prominent upregulation of particularly PPTS expression (20–23-fold), accounting for the observed enhancement in protopanaxatriol ginsenosides. However, none of the elicitors led to successful enhancement in in vitro anthocyanin accumulation as compared to control values.     

Copper-Induced Modulation of Biomass Growth,Physiological Parameters,Bioactive Centellosides,and Expression of Biosynthetic Pathway Genes in an Important Medicinal Herb, <Emphasis Type="Italic">Centella asiatica</Emphasis>

Hydroponically established Centella asiatica plants were studied under different concentrations of copper (0, 0.32,1.6, and 3.2 µM) for their morphological, physiological, and biochemical characteristics. The plants grown in the medium without any exogenous supply of copper showed improved biomass accumulation with maximum fresh weight (FW?=?24.7 g plant^?1) and dry weight (DW?=?2.35 g plant^?1). The total chlorophyll content, leaf number, and the leaf area were higher (0.27 mg g^?1 DW, 20 and 100.54 cm²) in the plants grown under copper-deficient conditions. The toxic effects of increased levels of copper were evident by significant inhibition in growth and other morphological parameters. Copper treatment showed an increase in malondialdehyde (MDA) content and SOD activity. Bioactive phytochemical profiling using HPLC analysis revealed that higher levels of copper (1.6 and 3.2 µM) inhibit the accumulation of total centelloside content. The differential accumulation of centelloside content was further validated by the consistent pattern of expression of key pathway genes related to centelloside production in copper-treated C. asiatica plants. The study unveiled some of the important facts associated with the mechanism of copper tolerance in this important medicinal herb C. asiatica. The findings of the present study can be further used to provide better production of high value, in demand centellosides.