Biology subjects

De, K.

Publications and source records attributed to De, K..

8 recordsLinked to original sources

bioRxiv2024

History of recurrent short and long-term coral bleaching events in Indian coral reefs: a a systematic review of contrasting bleaching patterns, lessons learned, and future directions

Climate change has intensified coral bleaching events, leading to widespread coral mortality and threatening the coral reef survival worldwide. However, species susceptibility patterns to bleaching differ spatially and temporally, making it crucial to understand bleaching impact and species susceptibility patterns across latitudinal ranges, particularly from understudied locations. We critically reviewed 23 years of bleaching episodes on Indian coral reefs (four major reefs and other patch reefs) reported from 1998 to 2020 to understand the geographical footprint of bleaching patterns, species susceptibility differences, and their impact. We found that all four major Indian reef systems (Gulf of Kachchh, Gulf of Mannar, Lakshadweep, and the Andaman Islands) have experienced three major bleaching episodes (1998, 2010, and 2016) and multiple short-term bleaching events. Short-term bleaching events (DHWs> four weeks) created differences in species susceptibility, but the disparity among species diminished to long-term bleaching events (DHWs <4 weeks) in all reef sites. Acropora, Porites, Pocillopora, Montipora, and Turninaria in the Gulf of Mannar, Porites, and Favia in the Gulf of Kachchh, and Acropora in the Andaman and Lakshadweep were the most vulnerable genera during all the bleaching events. In terms of recovery, Porites and other massive forms recovered better than branching forms. Furthermore, species susceptibility pattern analysis (winners vs. losers) to 2016 long-term bleaching events found conflicting results from studies (one-time surveys) in the same area. This result indicates that a one-time survey (survey timing) influences results as bleaching events lengthen, necessitating repeated surveys to determine winners and losers. Although inconsistent data from different study sites makes it difficult to create predictive models, data collected over the past 23 years provides critical insight into coral community susceptibility patterns and bleaching impacts, underscoring the need for systematic, uniform surveys in the future.

ecology↗

bioRxiv2023

The Plasminogen-Apple-Nematode (PAN) domain suppresses JA/ET defense pathways in plants

Suppression of immune response is a phenomenon that enables biological processes such as gamete fertilization, cell growth, cell proliferation, endophyte recruitment, parasitism, and pathogenesis. Here, we show for the first time that the Plasminogen-Apple-Nematode (PAN) domain present in G-type lectin receptor-like kinases is essential for immunosuppression in plants. Defense pathways involving jasmonic acid and ethylene are critical for plant immunity against microbes, necrotrophic pathogens, parasites, and insects. Using two Salix purpurea G-type lectin receptor kinases, we demonstrated that intact PAN domains suppress jasmonic acid and ethylene signaling in Arabidopsis and tobacco. Variants of the same receptors with mutated residues in this domain could trigger induction of both defense pathways. Assessment of signaling processes revealed significant differences between receptors with intact and mutated PAN domain in MAPK phosphorylation, global transcriptional reprogramming, induction of downstream signaling components, hormone biosynthesis and resistance to Botrytis cinerea. Further, we demonstrated that the domain is required for oligomerization, ubiquitination, and proteolytic degradation of these receptors. These processes were completely disrupted when conserved residues in the domain were mutated. Additionally, we have tested the hypothesis in recently characterized Arabidopsis mutant which has predicted PAN domain and negatively regulates plant immunity against root nematodes. ern1.1 mutant complemented with mutated PAN shows triggered immune response with elevated WRKY33 expression, hyperphosphorylation of MAPK and resistant to necrotrophic fungus Botrytis cinerea. Collectively, our results suggest that ubiquitination and proteolytic degradation mediated by the PAN domain plays a role in receptor turn-over to suppress jasmonic acid and ethylene defense signaling in plants.

plant biology↗

bioRxiv2022

Split selectable marker mediated gene stacking in plants

Plant synthetic biology and genetic engineering depend on the controlled expression of transgenes of interest, which relies heavily on the use of Agrobacterium-mediated transformation. Here we establish a novel split selectable marker system using protein splicing elements called "inteins" for Agrobacterium-mediated co-transformation in plants. This method enables robust co-transformation in Arabidopsis and poplar, providing a novel strategy for the simultaneous insertion of multiple genes into both herbaceous and woody plants.

plant biology↗

bioRxiv2022

Bimodal pilot study on inner speech decoding reveals the potential of combining EEG and fMRI

The recognition of inner speech, which could give a voice to patients that have no ability to speak or move, is a challenge for brain-computer interfaces (BCIs). A shortcoming of the available datasets is that they do not combine modalities to increase the performance of inner speech recognition. Multimodal datasets of brain data enable the fusion of neuroimaging modalities with complimentary properties, such as the high spatial resolution of functional magnetic resonance imaging (fMRI) and the temporal resolution of electroencephalography (EEG), and therefore are promising for decoding inner speech. This paper presents the first publicly available bimodal dataset containing EEG and fMRI data acquired nonsimultaneously during inner-speech production. Data were obtained from four healthy, right-handed participants during an inner-speech task with words in either a social or numerical category. Each of the 8-word stimuli were assessed with 40 trials, resulting in 320 trials in each modality for each participant. The aim of this work is to provide a publicly available bimodal dataset on inner speech, contributing towards speech prostheses.

neuroscience↗

bioRxiv2022

Rethinking the Methods and Algorithms for Inner Speech Decoding - and Making them Reproducible

This study focuses on the automatic decoding of inner speech using noninvasive methods, such as electroencephalography (EEG)). While inner speech has been a research topic in philosophy and psychology for half a century, recent attempts have been made to decode nonvoiced spoken words by using various brain-computer interfaces. The main shortcomings of existing work are reproducibility and the availability of data and code. In this work, we investigate various methods (using Convolutional Neural Network (CNN), Gated Recurrent Unit (GRU), Long Short-Term Memory Networks (LSTM)) for the detection task of 5 vowels and 6 words on a publicly available EEG dataset. The main contributions of this work are (1) subject dependent vs. subject-independent approaches, (2) the effect of different preprocessing steps (Independent Component Analysis (ICA), down-sampling and filtering), and (3) word classification (where we achieve state-of-the-art performance on a publicly available dataset). Overall we achieve a performance accuracy of 35.20% and 29.21% when classifying 5 vowels and 6 words respectively in a publicly available dataset, using our tuned iSpeech-CNN architecture. All of our code and processed data are publicly available to ensure reproducibility. As such, this work contributes to a deeper understanding and reproducibility of experiments in the area of inner speech detection.

neuroscience↗

bioRxiv2021

Mutating novel interaction sites in NRP1 reduces SARS-CoV-2 spike protein internalization

The global pandemic of Coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 has become a severe global health problem because of its rapid spread(1). Both angiotensin-converting enzyme 2 and neuropilin 1 provide initial viral binding sites for SARS-CoV-2 (2, 3). Here, we show that three cysteine residues located in a1/a2 and b1 domains of neuropilin 1 are necessary for SARS-CoV-2 spike protein internalization in human cells. Mutating cysteines C82, C104 and C147 altered neuropilin 1 stability and binding ability as well as cellular internalization and lysosomal translocation of the spike protein. This resulted in up to 4 times reduction in spike protein load in cells for the original, alpha and delta SARS-CoV-2 variants even in the presence of the endogenous angiotensin-converting enzyme 2 receptor. Transcriptome analysis of cells transfected with mutated NRP1 revealed significantly reduced expression of genes involved in viral infection and replication, including eight members of the ribosomal protein L, ten members of ribosomal protein S and five members of the proteasome {beta} subunit family proteins. We also observed higher expression of genes involved in suppression of inflammation and endoplasmic reticulum associated degradation. These observations suggest that these cysteines offer viable targets for therapies against COVID-19.

genetics↗

bioRxiv2021

Core cysteine residues in the PAN domain are critical for HGF/c-MET signaling

The Plasminogen-Apple-Nematode (PAN) domain, with a core of four to six cysteine residues, is found in > 28,000 proteins across 959 genera but its role in protein function is not fully understood. The PAN domain was initially characterized to be present in numerous proteins including hepatocyte growth factor (HGF). Dysregulation of HGF-mediated signaling results in numerous deadly cancers. All biological impacts of HGF in cell proliferation are triggered by binding of HGF to its cell surface receptor, cellular mesenchymal-epidermal transition (c-MET). Here, we show that four PAN domain cysteine residues are essential for HGF/c-MET signaling. Mutating these residues resulted in retardation of perinuclear localization, cellular internalization of HGF and its receptor, c-MET, and c-MET ubiquitination. Our observations indicate that the PAN domain of HGF is required for the c-MET binding and subsequent c-MET autophosphorylation and phosphorylation of its downstream targets, protein kinase B (AKT), extracellular signal-regulated kinase (ERK), and signal transducer and activator of transcription 3 (STAT3). Furthermore, transcriptional activation of HGF/c-MET signaling-related genes including matrix metalloproteinase-9 (MMP9), ETS translocation variant 1, 4, and 5 (ETV1, ETV4, ETV5), and early growth response 1 (EGR1) was impaired and cell proliferation was attenuated. These results suggest that core cysteine residues in the PAN domain are critical for HGF/c-MET interaction, c-MET mediated signal transduction, and cell survival. Thus, targeting the PAN domain of HGF may represent a mechanism for selectively regulating the binding and activation of the c-MET pathway. SignificanceHGF/c-MET signaling induces multifunctional cellular responses. Dysregulation of HGF/c-MET signaling cascade can lead to tumorigenesis by transforming normal cells to tumor cells. This work defines the importance of core cysteine residues in the PAN domain of HGF in downstream activation of HGF/c-MET signaling. To understand the role of cysteines in the PAN domain, PAN mutants of HGF were used to stimulate c-MET signaling in cells and the impact was delineated by determining phosphorylation and transcription of downstream targets. Mutations in core cysteines in the HGF-PAN domain completely blocked downstream phosphorylation and perinuclear accumulation of c-MET. These results suggest an indispensable role for the cysteine-rich PAN domain in HGF/c-MET interaction and could set the stage for future therapies that selectively disrupt the MET signaling cascade with limited off-target effects in tumors overexpressing HGF/c-MET.

cell biology↗

bioRxiv2019

Chk1 Phosphorylates Cdh1 to Promote SCFβTRCP-Dependent Degradation of Cdh1 During S-Phase

The interplay of the Anaphase-Promoting Complex/Cyclosome (APC/C) and Skp1-Cul1-F-box (SCF) E3 ubiquitin ligases is necessary for controlling cell cycle transitions and checkpoint responses, which are critical for maintaining genomic stability. Yet, the mechanisms underlying the coordinated activity of these enzymes are not completely understood. Recently, Cyclin A- and Plk1- mediated phosphorylation of Cdh1 was demonstrated to trigger its ubiquitination by SCF{beta}TRCP at the G1/S transition. However, Cyclin A-Cdk and Plk1 activities peak in G2 so it is unclear why Cdh1 is targeted at G1/S but not in G2. Here, we show that phosphorylation of Cdh1 by Chk1 contributes to its recognition by SCF{beta}TRCP, promotes efficient S-phase entry, and is important for cellular proliferation. Conversely, Chk1 activity in G2 inhibits Cdh1 accumulation. Overall, these data suggest a model whereby the rise and fall of Chk1 activity is a key factor in the feedback loop between APC/CCdh1 and the replication machinery that enhances the G1/S and S/G2 transitions, respectively.

cell biology↗