Tuning Membrane Thickness Fluctuations in Model Lipid Bilayers

Membrane thickness fluctuations have been associated with a variety of critical membrane phenomena, such as cellular exchange, pore formation, and protein binding, which are intimately related to cell functionality and effective pharmaceuticals. Therefore, understanding how these fluctuations are controlled can remarkably impact medical applications involving selective macromolecule binding and efficient cellular drug intake. Interestingly, previous reports on single-component bilayers show almost identical thickness fluctuation patterns for all investigated lipid tail-lengths, with similar temperature-independent membrane thickness fluctuation amplitude in the fluid phase and a rapid suppression of fluctuations upon transition to the gel phase. Presumably, in vivo functions require a tunability of these parameters, suggesting that more complex model systems are necessary. In this study, we explore lipid tail-length mismatch as a regulator for membrane fluctuations. Unilamellar vesicles of an equimolar mixture of dimyristoylphosphatidylcholine and distearoylphosphatidylcholine molecules, with different tail-lengths and melting transition temperatures, are used as a model system for this next level of complexity. Indeed, this binary system exhibits a significant response of membrane dynamics to thermal variations. The system also suggests a decoupling of the amplitude and the relaxation time of the membrane thickness fluctuations, implying a potential for independent control of these two key parameters.     

A global meta‐analysis of exotic versus native leaf decay in stream ecosystems

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Staying in situ or shifting range under ongoing climate change: A case of an endemic herb in the Himalaya-Hengduan Mountains across elevational gradients

Aim

How species respond to ongoing climate change has been a hot research topic, especially with the controversy in shifting range (movement) or persisting in local habitat (in situ) as the primary response. Assessing the relative roles of range shifts, phenotypic plasticity and genetic adaptation helps us predict the evolutionary fate of species. We aim to explore the evolutionary strategies of plants under climate change from a keystone herb in alpine ecosystems, Mirabilis himalaica, along its elevational gradient.

Location

Himalaya-Hengduan Mountains, China.

Methods

We combined evidence from population genomics and ecological data in both space and time to investigate the state of “staying” or “moving”. We identified migration events by assessing historical and contemporary gene flow and changes in species distribution. Morphological variation was compared by measuring five traits using specimen data. Moreover, we explored climate-driven genetic variation and local selection regimes acting on populations in the alpine landscape along an elevational gradient.

Results

Our results argue that staying in situ by morphological variation and local genetic evolution rather than range shifting plays an important role in M. himalaica response to climate change. We first found trace evidence of upward or climatic-driven shifting along an elevational gradient, although asymmetric gene flow was restricted within microenvironments of mid-elevational populations. Furthermore, morphological variation comparisons revealed clinal variation, as resource allocation showed a declining pattern in vegetative growth but increased reproductive growth with increasing elevation. Outlier tests and environment association analyses indicated adaptative loci primarily related to thermal-driven selection and continuous adaptations to high elevation in the Himalaya-Hengduan Mountains.

Main Conclusions

Our findings show M. himalaica may persist in local habitats rather than shifting range under climate change, exhibiting a low risk of genomic vulnerability in current habitats. This study has important implications in improving our understanding of the evolutionary response in alpine plants to climate change.     

Thunbergia laurifolia leaf extract partially recovers lead-induced renotoxicity through modulating the cell signaling pathways

This research investigated the reno-protective effect of Thunbergia laurifolia Linn. (TL) in a lead-induced toxicity test through the modulation of cell signaling pathways. The study carried out to evaluate the effect of TL leaf extracts in Swiss Albino mice exposed to lead acetate (PbAc). Prior to in vivo study, a probable kidney-protective effect of the plant leaf extract was presumed through an activity-specific (PASS) molecular docking analysis. In animal model study, albino mice were divided in seven groups and co-treated with PbAc and TL (100, 200 mg/kgBW) or vitamin E (100 mg/kgBW) for 38 days, whereas the untreated control, TL control, and vehicle control groups received sodium acetate, PbAc, sodium acetate plus mineral oil, respectively. At the end of treatment, blood and kidney tissue were collected for investigating Pb concentration, estimating biochemical profile, evaluating oxidative stress and inflammatory parameters. The histopathological change of kidney along with apoptosis was assessed from kidney sections using H & E staining and TUNEL assay. Pb-exposed mice were found to be increased concentration of Pb in the blood and kidney sample, which further led to increased MDA levels in the plasma, blood, and tissue. Followed by kidney damage, increased expression of TNF-α, iNOS, and COX-2 in kidney tissues were noticed, which were related to elevated TNF-α in the systemic circulation of Pb-treated mice. Co-treatment with TL or vitamin E significantly reduced altered structure and apoptosis of kidney tissues. Downregulation of inflammatory markers especially TNF-α, iNOS, and COX-2 with simultaneous improvement of renal function through reduced plasma BUN and creatinine levels demonstrate that TL act as a potential dietary supplement to detoxify Pb in kidney showing an antioxidant and anti-inflammatory effect.     

Analysis of the Coat Protein Gene of Indian Strain of Apple Stem Grooving Virus

A survey was undertaken in the temperate fruit growing regions of Himachal Pradesh (HP) and Jammu & Kashmir (J&K). Apple stem grooving virus (ASGV), a Capillovirus, was detected in different cultivars of apple, nectarines, plum, cherry, quince and apricot by double antibody sandwich ELISA (DAS-ELISA). The coat protein (CP) gene sequence of an amplicon produced by RT-PCR, confirmed the association of ASGV in apple cultivar Starkrimson, collected from Himachal Pradesh. The CP of Indian ASGV isolate shared 100 % sequence identity with a Brazilian isolate (AF438409). Sequence analysis by Recombination Detection Program (RDP2) indicated no recombination event for the Indian isolate. However, recombination was detected in Chinese, Korean and Citrus tatter leaf virus-Taiwan (CTLV) strains of ASGV. The study describes first report of ASGV infection in India and characterization of its CP gene.     

Multi-modal Binding of a ‘Self’ Peptide by HLA-B*27:04 and B*27:05 Allelic Variants,but not B*27:09 or B*27:06 Variants: Fresh Support for Some Theories Explaining Differential Disease Association

A self-derived-peptide with the same amino acid sequence (N-RRYLENGKETLQR-C) as residues 169–181 of the human leukocyte antigen (HLA) B27 heavy chain is known to bind to MHC Class I complexes containing the HLA-B27 heavy chain. This observation has been invoked previously in at least two different (but related) molecular explanations for the disease-association of the HLA-B27 allele. Here, we use a combination of fluorescence polarization, competitive inhibition and gel filtration chromatographic studies to show that a fluorescently-labeled peptide of the above sequence binds to two disease-associated subtypes of HLA-B27 (namely HLA-B*27:04 and HLA-B*27:05) but not to non-disease-associated subtypes (HLA-B*27:06 or HLA-B*27:09). This differential binding behavior is seen both in (a) peptide binding to complexes of heavy chain (HLA-B27) and light chain (β₂ microglobulin), and in (b) peptide binding to β₂ microglobulin-free heavy chains in the aggregated state. Such subtype-specific differences are not seen with two other control peptides known to bind to HLA-B27. Our results support the likelihood of differential peptide binding holding at least one of the keys to HLA-B27’s disease association.