Biology subjects

Bhattacharyya, A.

Publications and source records attributed to Bhattacharyya, A..

4 recordsLinked to original sources

bioRxiv2018

Redox fluctuations control the coupled cycling of iron and carbon in tropical forest soils

Oscillating redox conditions are the norm in tropical soils; driven by an ample supply of reductants, high moisture, microbial oxygen consumption, and finely textured clays that limit diffusion. Yet the net result of variable soil redox regimes on iron-organic matter (Fe-OM) associations in tropical soils owing to changing climate is poorly understood. Using a 44-day redox incubation experiment with humid tropical soils from Puerto Rico, we examined patterns of Fe and C transformation under four redox regimes: static anoxic, flux 4-day (4d oxic, 4d anoxic), flux 8-day (8d oxic, 4d anoxic) and static anoxic. Prolonged anoxia promoted reductive dissolution of Fe-oxides and an increase in short-range ordered (SRO) Fe oxides. Preferential dissolution of this less-crystalline Fe pool was evident immediately following a shift in bulk redox status (oxic to anoxic), and coincided with increased dissolved organic carbon, presumably due to acidification or direct release of OM from dissolving Fe(III) mineral phases. Average nominal oxidation state of water-soluble carbon was lowest under persistent anoxic conditions, suggesting more reduced OC is microbially preserved under reducing conditions. Anoxic soil compounds had high H/C values (similar to lignin-like metabolites) whereas oxic soil compounds had higher O/C values, akin to tannin- and cellulose-like components. Cumulative respiration derived from native soil organic carbon was highest in static oxic soils. These results highlight the volatility of mineral-OM interactions in tropical soils, and suggest that short-term impacts of shifting soil O2 availability control exchanges of C between mineral-sorbed and aqueous pools, implying that the periodicity of low-redox moments may control the fate of C in wet tropical soils.\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=121 SRC=\"FIGDIR/small/312108_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (23K):\norg.highwire.dtl.DTLVardef@add07borg.highwire.dtl.DTLVardef@15269bforg.highwire.dtl.DTLVardef@19ca034org.highwire.dtl.DTLVardef@1d9d793_HPS_FORMAT_FIGEXP M_FIG Toc Art C_FIG

ecology↗

bioRxiv2018

A CRISPR/Cas9 based strategy to manipulate the Alzheimer’s amyloid pathway

The gradual accumulation of amyloid-{beta} (A{beta}) is a neuropathologic hallmark of Alzheimers disease (AD); playing a key role in disease progression. A{beta} is generated by the sequential cleavage of amyloid precursor protein (APP) by {beta}- and {gamma}-secretases, with BACE-1 ({beta}-site APP cleaving enzyme-1) cleavage as the rate limiting step 1-3. CRISPR/Cas9 guided gene-editing is emerging as a promising tool to edit pathogenic mutations and hinder disease progression 4,5,6 However, few studies have applied this technology to neurologic diseases 7-9. Besides technical caveats such as low editing efficiency in brains and limited in vivo validation 7, the canonical approach of mutation-correction would only be applicable to the small fraction of neurodegenerative cases that are inherited (i.e. < 10% of AD, Parkinsons, ALS); with a new strategy needed for every gene. Moreover, feasibility of CRISPR/Cas9 as a therapeutic possibility in sporadic AD has not been explored. Here we introduce a strategy to edit endogenous APP at the extreme C-terminus and reciprocally manipulate the amyloid pathway - attenuating {beta}-cleavage and A{beta}, while up-regulating neuroprotective a-cleavage. APP N-terminus, as well as compensatory APP homologues remain intact, and key physiologic parameters remain unaffected. Robust APP-editing is seen in cell lines, cultured neurons, human embryonic stem cells/iPSC-neurons, and mouse brains. Our strategy works by limiting the physical association of APP and BACE-1, and we also delineate the mechanism that abrogates APP/BACE-1 interaction in this setting. Our work offers an innovative cut and silence gene-editing strategy that could be a new therapeutic paradigm for AD.

neuroscience↗

bioRxiv2018

Aberrant calcium signaling in astrocytes inhibits neuronal excitability in a human Down syndrome stem cell model

Down syndrome (DS) is a devastating genetic disorder causing severe cognitive impairment. The staggering array of effects associated with an extra copy of human chromosome 21 (HSA21) complicates mechanistic understanding of DS pathophysiology. We developed an in vitro system to examine the interplay of neurons and astrocytes in a fully recapitulated HSA21 trisomy model differentiated from DS patient-derived induced pluripotent stem cells (iPSCs). By combining calcium imaging with genetic approaches, we utilized this system to investigate the functional defects of DS astroglia and their effects on neuronal excitability. We found that, compared with control isogenic astroglia, DS astroglia exhibited more-frequent spontaneous calcium fluctuations, which reduced the excitability of co-cultured neurons. DS astrocytes exerted this effect on both DS and healthy neurons. Neuronal activity could be rescued by abolishing astrocytic spontaneous calcium activity either chemically by blocking adenosine-mediated astrocyte-neuron signaling or genetically by knockdown of inositol triphosphate (IP3) receptors or S100{beta}, a calcium binding protein coded on HSA21. Our results suggest a novel mechanism by which DS alters the function of astrocytes, which subsequently disturbs neuronal excitability. Furthermore, our study establishes an all-optical neurophysiological platform for studying human neuron-astrocyte interactions associated with neurological disorders.\n\nSignificant statementDown syndrome (DS) is the most common genetic disorder caused by trisomy of chromosome 21 (HSA21). Problems with cognitive impairment, have not been properly addressed due to the inability to fully recapitulate HSA21, which is further confounded by the snapshot views of morphological changes of brain cells in isolation obtained from current studies. The brain develops neural networks consisting of neurons and glial cells that work together. To understand how DS affects the neural networks, we used DS patient-derived stem cells and calcium imaging to investigate functional defects of DS astrocytes and their effects on neuronal excitability. Our study has significant implication in understanding functional defects during brain development underlying DS.

neuroscience↗

bioRxiv2017

Emerging Electrical Properties of Graphene incorporated Photosynthetic Biofilms

We report emergence of a new electrical material by growing photosynthetic biofilm on a Dirac material, graphene. The material showed new conducting as well as semiconducting properties. Frequency dependent capacitive spectra further indicated presence of electrical isosbestic points(at 0.8 and 9MHz), implying two state dieletric transitions at critical frequencies. A notable reult was a Schottky diode like behavior in the IV curve. Voltage dependent conductance with conductance peaks near the Schottky diode threshold was observed. We obtained facilitated growth of photosynthetic biofilm in presence of graphene. Lastly higher bacterial metabolism i was seen in the biofilm in contact with graphene as compared to its normal growth condition. For this zero band gap Dirac material this can only be interpreted as coupling of the electron transport chain of the bacterial biofilm and the graphene electron cloud.

biophysics↗