Biology subjects

Kaur, G.

Publications and source records attributed to Kaur, G..

At least 55 records · Page 3Linked to original sources

bioRxiv2022

Transcriptome and biochemical analysis pinpoint multi-layered molecular processes associated with iron deficiency tolerance in hexaploid wheat

Iron (Fe) is an essential nutrient for plants that is indispensable for many physiological activities. Although few genotypes were identified with contrasting tolerance to Fe deficiency, the molecular insight into the distinct biochemical and transcriptional responses determining the trait is poorly known. This study aimed to identify the molecular and biochemical basis for the contrasting Fe deficiency tolerance in wheat genotype showing tolerance to Fe deficiency (cv. Kanchan-KAN) compared to susceptible (cv. PBW343-PBW) cultivar. Under Fe deficiency, the KAN show delayed chlorosis, high SPAD values and low malondialdehyde activity compared to PBW. The shoot transcriptomics studies show that a large set of genes for photosynthetic pathways were highly induced in PBW, suggesting its sensitivity to Fe deficiency. Although, under Fe deficiency, both the cultivars show distinct molecular re-arrangements, including high expression of genes involved in Fe uptake (including membrane transporters) and mobilization, the gene expression level was higher in KAN. Furthermore, the KAN cultivar also shows high ubiquitination activity in the shoot tissue suggesting a high turnover of proteins in the tolerant cultivar. These observations were also co-related with the high root phytosiderophores biosynthesis and its release that contributes to the enhanced Fe translocation index in KAN. Overall, our work provides the key link to understanding the mechanistic insight for the Fe deficiency tolerance in hexaploid wheat. This will enable wheat breeders to select genotypes for better Fe use efficiency for agriculture.

plant biology↗

bioRxiv2022

Asymmetric expression of homoeologous genes in wheat roots modulates the early phase of iron-deficiency signalling

Iron (Fe) limitation leads to dramatic changes in gene expression in plants, to induce iron uptake and mobilization, while at the same time restrict Fe-dependent metabolism and growth. Although transcriptional changes in response to Fe deficiency have recently been charted in wheat, this was performed at a stage when photosynthesis and growth were severely impacted, confounding primary and secondary responses. Here, we specifically uncover the transcriptional landscape of wheat roots during the early stages of the Fe deficiency response (4 and 8 days) and after Fe resupply. Root growth was significantly inhibited at day 4, but chlorosis only became apparent on day 8. The number of differentially expressed genes increased from 1386 on day 4 to 3538 on day 8, with an overlap of 2006 genes. Genes with dynamic changes in expression patterns include membrane transporters and transcription factors shown to be involved in Fe homeostasis in other plant species. Comparative analysis of the Fe deficiency response at 4, 8 and 20 days identified a core set of Fe-regulated genes. Analysis of the expression of homoeologs suggests an increase in induction bias at 8 days compared to 4 days particularly, A genome contributing high at 4 days and the A+D genomes at 8 days. Overall, our work will contribute towards fundamental knowledge of the Fe signalling networks in wheat and point to the interplay of the three sub-genomes in this hexaploid species to fine tune the transcriptional response.

plant biology↗

bioRxiv2022

An auto-inhibited state of protein kinase G and implications for selective activation

Cyclic GMP-dependent protein kinases (PKGs) are key mediators of the nitric oxide/cGMP signaling pathway that regulates biological functions as diverse as smooth muscle contraction, cardiac function, and axon guidance. Campaigns targeting nitric oxide synthases and cyclic nucleotide phosphodiesterases in this signaling axis suggest that understanding how cGMP differentially triggers mammalian PKG isoforms could lead to new therapeutics that inhibit or activate PKGs. Alternate splicing of PRKG1 transcripts confers distinct leucine zippers, linkers, and auto-inhibitory pseudo-substrate sequences to PKG I and I{beta} that result in isoform-specific activation properties, but the mechanism of enzyme auto-inhibition and its alleviation by cGMP is still not well understood. Here we present a crystal structure of PKG I{beta} in which the auto-inhibitory sequence and the cyclic nucleotide binding domains are bound to the catalytic domain, providing a snapshot of the auto-inhibited state. Specific contacts between the PKG I{beta} auto-inhibitory sequence and the enzyme active site help explain isoform-specific activation constants and the effects of phosphorylation in the linker. We also present a crystal structure of a PKG I cyclic nucleotide binding domain with an activating mutation linked to Thoracic Aortic Aneurysms and Dissections. Similarity of this structure to wild type cGMP-bound domains and differences with the auto-inhibited enzyme provide a mechanistic basis for constitutive activation. We show that PKG I{beta} auto-inhibition is mediated by contacts within each monomer of the native full-length dimeric protein, and using the available structural and biochemical data we develop a model for the regulation and activation of PKGs.

biochemistry↗

bioRxiv2022

Visual Perception of 3D Space and Shape In Time - Part IV: 3D Shape Recognition by 3D Rotation

Human vision has a remarkable ability to recognize complex 3D objects such as faces that appear at any size and 3D orientations at any 3D location. If we initially memorize a face only with a normalized size upfront at the object center, the direct comparison between the one-sized memory and an incoming new image would demand tremendous mental frame translations in 7D. How can we perform such a demanding task so promptly as we experience it in our daily lives? This paper specifically addresses the recognition of human faces with arbitrary 3D orientation in the [Roll, Yaw, Pitch] axes. According to our new model of NHT (Neural Holography Tomography), space is represented by time utilizing the phase of the alpha brainwave. This principle should be applicable to any mental rotation in 3D; thus, it predicts that extra time is required to perceive a rotated face to revolve it back to upright by the constant-speed alpha wave. To assess this hypothesis, we designed a reaction time (RT) experiment, where participants were first asked to memorize sets of upright unfamiliar faces. Following the memorization phase, similar stimuli with a wide range of rotating faces in 3D were presented, and RTs were recorded. As expected, the memorized upfront face was the fastest RT. The excess of the RT was observed proportional to the rotating angle in all [Roll, Yaw, Pitch] axes. Roll had the flattest slope, whereas upper Pitch was the steepest. We suspect that Roll is the swiftest mental operation because it can be conducted by the linear frame translation on the log-polar retinotopy of the visual cortex.

neuroscience↗

bioRxiv2022

Deep proteome analysis of plasma reveals novel biomarkers of mild cognitive impairment and Alzheimer's disease: A longitudinal study

Ageing is the primary risk factor for AD; however, there is a poor understanding of the biological mechanisms by which the ageing process contributes to the development of AD in some individuals, while others progress to advanced age with relatively little AD neuropathology. To halt the progression of AD, the preclinical stage of neurodegeneration (before the onset of clinical symptoms) is anticipated to be the more effective time point for applying potentially disease-modifying interventions in AD. The main objective of this study was to understand the age and disease related proteomic changes are detectable in plasma, based on retrospective analysis of longitudinal data and cross-sectional analyses of clinically diagnosed cases. We conducted an in-depth plasma proteomics analysis using intensive depletion of high-abundant plasma proteins using the Agilent multiple affinity removal liquid chromatography (LC) column-Human 14 (Hu14) followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS PAGE) technique. In this study, we have begun to address the following questions; (1) differences in plasma proteomic profiles between normal ageing, vs ageing with progress to cognitive decline (MCI) or disease (dementia, probable AD), (2) cross-sectional analysis of baseline data, when all subjects are clinically identified as cognitively normal, provides insight into the preclinical changes which precede subsequent progression to AD and potentially provide early biomarkers, and (3) comparison of plasma at the point of progression to clinically diagnosed onset of cognitive decline or AD, can provide potential plasma biomarkers to facilitate clinical diagnosis. Furthermore, our findings also identified some proteins previously discovered in AD CSF and brain proteomics signatures that could provide clinically meaningful information. We identified differentially expressed proteins which were associated with several biological and molecular processes that may serve as therapeutic targets and fluid biomarkers for the disease.

neuroscience↗

bioRxiv2022

Impact of APOE e3 and e4 genotypes on plasma proteome signatures in Alzheimer's disease

The {varepsilon}4 allele of the apolipoprotein E (APOE) gene is a high-risk factor for Alzheimers disease (AD). However, approximately 25%-40% of patients with AD do not carry the APOE{varepsilon}4 allele, and the pathophysiological mechanisms underlying AD are less evident in these individuals. The main objective of this study was to understand better the changes in plasma that may contribute to disease pathogenesis in AD and how APOE{varepsilon}3 and APOE{varepsilon}4 contribute to biomarker profiles in AD. We conducted an in-depth plasma proteomics analysis using intensive depletion of high-abundant plasma proteins using the Agilent multiple affinity removal liquid chromatography (LC) column-Human 14 (Hu14) followed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS PAGE) technique. In this study, we identified a high number of protein expression alterations in plasma which were found uniquely in APOE{varepsilon}3 and APOE{varepsilon}4 carriers. These differentially expressed proteins (DEPs) were associated with several molecular functions, including complement cascade, glycolysis, metabolism, plasma lipoprotein assembly, remodelling, and clearance. In addition to unique changes in both APOE genotypes, many proteins were also dysregulated in the presence of both APOE{varepsilon}3 and APOE{varepsilon}4 genotypes depicting the involvement of these proteins in the pathogenesis of AD regardless of the APOE genotypes. We also compared the plasma proteomes of{varepsilon} 4 and{varepsilon} 3 carriers in normal controls, which provided insight into factors that may provide protection from progression to AD despite the presence of the{varepsilon} 4 allele. Furthermore, our findings also identified some proteins previously discovered in AD CSF and brain proteomics signatures that could provide clinically meaningful information.

neuroscience↗

bioRxiv2021

Plakoglobin and HMGB1 mediate intestinal epithelial cell apoptosis induced by Clostridioides difficile TcdB

Clostridioides difficile infection (CDI) is the leading cause of antibiotic-associated intestinal disease, resulting in severe diarrhea and fatal pseudomembranous colitis. TcdB, one of the essential virulence factors secreted by this bacterium, induces host cell apoptosis through a poorly understood mechanism. Here, we performed an RNAi screen customized to Caco-2 cells, a cell line model of the intestinal epithelium, to discover host factors involved in TcdB-induced apoptosis. We identified plakoglobin, also known as junction plakoglobin (JUP) or {gamma}-catenin, a member of the catenin family, as a novel host factor, and a previously known cell death-related chromatin factor, high mobility group box 1 (HMGB1). Disruption of those host factors by RNAi and CRISPR resulted in resistance of cells to TcdB-mediated and mitochondria-dependent apoptosis. JUP was redistributed from adherens junctions to the mitochondria and colocalized with Bcl-XL after stimulation by TcdB, suggesting a role of JUP in cell death signaling through mitochondria. Treatment with glycyrrhizin, an HMGB1 inhibitor, resulted in significantly increased resistance to TcdB-induced epithelial damage in cultured cells and a mouse ligated colon loop model. These findings demonstrate the critical roles of JUP and HMGB1 in TcdB-induced epithelial cell apoptosis.

microbiology↗

bioRxiv2021

A Synthetic, Closed-Looped Gene Circuit for the Autonomous Regulation of RUNX2 Activity during Chondrogenesis

The transcription factor RUNX2 is a key regulator of chondrocyte phenotype during development, making it an ideal target for prevention of undesirable chondrocyte maturation in cartilage tissue engineering strategies. Here, we engineered an autoregulatory gene circuit (cisCXp-shRunx2) that negatively controls RUNX2 activity in chondrogenic cells via RNA interference initiated by a tunable synthetic Col10a1-like promoter (cisCXp). The cisCXp-shRunx2 gene circuit is designed based on the observation that induced RUNX2 silencing after early chondrogenesis enhances the accumulation of cartilaginous matrix in ATDC5 cells. We show that the cisCXp-shRunx2 initiates RNAi of RUNX2 in maturing chondrocytes in response to the increasing intracellular RUNX2 activity without interfering with early chondrogenesis. The induced loss of RUNX2 activity in turn negatively regulates the gene circuit itself. Moreover, the efficacy of RUNX2 suppression from cisCXp-shRunx2 can be controlled by modifying the sensitivity of cisCXp promoter. Finally, we show the efficacy of inhibiting RUNX2 in preventing matrix loss in human MSC-derived cartilage under conditions that induce chondrocyte hypertrophic differentiation, including inflammation. Overall, our results demonstrated that the negative modulation of RUNX2 activity with our autoregulatory gene circuit enhanced matrix synthesis and resists ECM degradation by reprogrammed MSC-derived chondrocytes in response to the microenvironment of the degenerative joint.

genetics↗

bioRxiv2021

Parental-fetal interplay of immune genes leads to intrauterine growth restriction

Intrauterine growth restriction (IUGR) of fetuses affects 5-10% of pregnancies and is associated with perinatal morbidity, mortality and long-term health issues. Understanding genetic predisposition to IUGR is challenging, owing to extensive gene polymorphisms, linkage disequilibrium, and maternal and paternal influence. Here, we demonstrate that the inhibitory receptor, KIR2DL1, expressed on maternal uterine natural killer (uNK) cells, in interaction with the paternally-inherited HLA-C*05, an HLA-C group 2 allotype, expressed on fetal trophoblast cells, causes IUGR in a humanised mouse model. Micro-CT imaging of the uteroplacental vasculature revealed reduced uterine spiral artery diameter and increased segment length, increasing fetal blood flow resistance. Single cell RNA-Seq from the maternal-fetal interface highlighted expression programs activated by KIR2DL1-induced IUGR in several placental cell types, including degradation of extracellular matrix components, angiogenesis, and uNK cell communication, suggesting a complex response underlying IUGR. As current IUGR treatments are insufficient, our findings provide important insight for drug development.

immunology↗

bioRxiv2021

p16-3MR: a novel model to study cellular senescence in cigarette smoke-induced lung injuries during aging

Cellular senescence and lung aging are associated with the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). COPD progresses with aging, and chronic smoking is the key susceptibility factor in lung pathological changes concurrent with biological aging. However, these processes involving cigarette smoke (CS)-mediated lung cellular senescence are difficult to distinguish. One of the impediments to study cellular senescence in relation to age-related lung pathologies is the lack of a suitable in vivo model. In view of this, we provide evidence that supports the suitability of p16-3MR mice to study cellular senescence in CS-mediated and age-related lung pathologies. p16-3MR mice has a trimodal reporter fused to the promoter of p16INK4a gene that enables detection, isolation and selective elimination of senescent cells, thus making it a suitable model to study cellular senescence. To determine its suitability in CS-mediated lung pathologies, we exposed young (12-14 months) and old (17-20 months) p16-3MR mice to 30-day CS exposure and studied the expression of senescent genes (p16, p21 and p53) and SASP-associated markers (MMP9, MMP12, PAI-1, and FN-1) in air- and CS-exposed mouse lungs. Our results showed that this model could detect cellular senescence using luminescence and isolate cells undergoing senescence with the help of tissue fluorescence in CS-challenged young and old mice. Our results from the expression of senescence markers and SASP-associated genes in CS-challenged young and old p16-3MR mice were comparable with increased lung cellular senescence and SASP in COPD. We further showed age-dependent alteration in the (i) tissue luminescence and fluorescence, (ii) mRNA and protein expressions of senescent markers and SASP genes, and (iii) SA-{beta}-gal activity in CS-challenged young and old p16-3MR mice as compared to their air controls. Overall, we showed that p16-3MR is a competent model to study cellular senescence in age-related pathologies and could help understand the pathobiology of cellular senescence in lung conditions like COPD and fibrosis.

pharmacology and toxicology↗

bioRxiv2021

Protein Phosphatase 1 regulates atypical chromosome segregation and cell polarity during mitotic and meiotic division in Plasmodium sexual stages

PP1 is a conserved eukaryotic serine/threonine phosphatase that regulates many aspects of mitosis and meiosis, often working in concert with other phosphatases, such as CDC14 and CDC25. The proliferative stages of the malaria parasite life cycle include sexual development within the mosquito vector, with male gamete formation characterized by an atypical rapid mitosis, consisting of three rounds of DNA synthesis, successive spindle formation with clustered kinetochores, and a meiotic stage during zygote to ookinete development following fertilization. It is unclear how PP1 is involved in these unusual processes. Using real-time live-cell and ultrastructural imaging, conditional gene knockdown, RNA-seq and proteomic approaches, we show that Plasmodium PP1 is implicated in both mitotic exit and, potentially, establishing cell polarity during zygote development in the mosquito midgut, suggesting that small molecule inhibitors of PP1 should be explored for blocking parasite transmission.

cell biology↗

bioRxiv2020

Applications of machine learning to solve genetics problems

The development of precise DNA editing nucleases that induce double-strand breaks (DSBs) - including zinc finger nucleases, TALENs, and CRISPR/Cas systems - has revolutionized gene editing and genome engineering. Endogenous DNA DSB repair mechanisms are often leveraged to enhance editing efficiency and precision. While the non-homologous end joining (NHEJ) and homologous recombination (HR) DNA DSB repair pathways have already been the topic of an excellent deal of investigation, an alternate pathway, microhomology-mediated end joining (MMEJ), remains relatively unexplored. However, the MMEJ pathways ability to supply reproducible and efficient deletions within the course of repair makes it a perfect pathway to be used in gene knockouts. (Microhomology Evoked Deletion Judication EluciDation) may be a random forest machine learning-based method for predicting the extent to which the location of a targeted DNA DSB are going to be repaired using the MMEJ repair pathway. On an independent test set of 24 HeLa cell DSB sites, MEDJED achieved a Pearson coefficient of correlation (PCC) of 81.36%, Mean Absolute Error (MAE) of 10.96%, and Root Mean Square Error (RMSE) of13.09%. This performance demonstrates MEDJEDs value as a tool for researchers who wish to leverage MMEJ to supply efficient and precise gene knock outs.

bioinformatics↗

bioRxiv2020

MTOR promotes basal cell carcinoma growth through atypical PKC

Advanced basal cell carcinomas (BCCs) are driven by the Hedgehog (HH) pathway and often possess inherent resistance to SMO inhibitors. Identifying and targeting pathways that bypass SMO could provide alternative treatments. Here, we use a combination of RNA-sequencing analysis of advanced BCC tumor-normal pairs and immunostaining of human and mouse BCC samples to identify an MTOR signature in BCC. Pharmacological inhibition of MTOR activity in BCC cells significantly reduces cell proliferation without affecting HH signaling. Similarly, treatment of Ptch1fl/fl; Gli1-CreERT2 mice with everolimus reduces tumor growth and aPKC activity, suggesting that MTOR promotes tumor growth by activating aPKC and demonstrating that suppressing MTOR could be a promising target for BCC patients.

cancer biology↗

bioRxiv2020

Anti-diabetic Potential of Aqueous Extract of Moringa oleifera, Ocimum gratissimum and Vernonia amygdalina in Alloxan-Induced Diabetic Rats

The incidence of diabetes mellitus (DM) is increasing globally and it is a major source of concern. This study was undertaken to assess the antidiabetic effect of the aqueous extract of Moringa oleifera, Ocimum gratissimum and Vernonia amygdalina. Sixty adult Wistar rats with body weight of 120-150 g were randomly assigned to groups of five rats each (n=12). Groups 1 served as normal control; Groups 2-5 were diabetic groups; group 2 served as negative control; group 3-5 received 100, 200 and 400 mg/kg of triherbal formula respectively. The body weight (BW) and fasting blood glucose level (FBSL) of the rats were monitored weekly. At the end of the experiment, all the rats were anaesthetized intraperitoneally (I.P) and blood samples were collected by cardiac puncture for biochemical analysis. There was an increase in the BW of the control group and varying doses of tri-herbal formation. It caused 88.0% decrease in FBSL; 371.7%, 386.6% and 296.0% with respect to 100, 200 and 400 mg/kg. Sub-chronic study of the effect of the extract showed a significant increase (P<0.05) in packed cell volume (PCV), white blood counts in rat induced diabetes. The histological studies showed that the diabetic rats with the architecture of the pancreas distorted, was restored to normal by the extract. Its LD50 was found to be greater than 1000 mg/kg indicating its safety in rats. This study has shown that triherbal formula has hypoglycemic and haematogical effects.

pharmacology and toxicology↗

bioRxiv2020

Evaluation Of Biochemical, Hematological And Antioxidant Properties In Mice Exposed To A Triherbal (Nigella sativa, Carica papaya And Boswellia sacra) Formular

Nigella sativa, Carica papaya and Boswellia sacra are medicinal plants in the commonly used in folkloric medicine due to the presence of its immense therapeutic properties. Fifty (50) female albino mice weighing between 15-22g were divided into five groups of 10 mice each. Animal in group 1 served as control group and were administered distilled water while animal in group 2 were given 2ml of cisplatin (orally). Animal in group 3-5 were given orally; 100 mg/kg (low dose), 200 mg/kg (medium dose) and 400 mg/kg (high dose) of triherbal preparation. The feeding regimens lasted for 28 days. After 28 days, mammary gland and blood samples were collected for haematological and antioxidant analysis. The triherbal formula decreased the GSH and MDA levels of mice treated with 100 mg/kg and 400 mg/kg doses compare to control. The measurement of total protein content, SOD and CAT increased in treated animals compared to control. However, RBC (Red Blood Cell) counts significantly decreased in the low, medium and high dose groups (0.95{+/-}0.08, 6.57{+/-}0.08 and 3.55{+/-}0.55 x 106 cells/mm3 respectively) compared to control (7.34{+/-}0.40) at P<0.05. Also, significant decreases (P<0.05) in the level of the total WBC (White Blood Cell) count, platelet count, PCV (Packed Cell Volume) and Hb (haemoglobin) concentration were observed. The decreases were dose dependent. The MCH (Mean Corpuscular Haemoglobin) and MCHC (Mean Corpuscular Haemoglobin Concentration) except MCV (Mean Corpuscular Volume) significantly decreased in treated group only. The triherbal formulation exhibited significant antioxidant activities showing increased levels of SOD, CAT and Protein content due to activation of the enzyme involve in detoxification of free radicals and decreased in the level of GSH and MDA due to accumulation of peroxides and H2O2. Also, decreased in haematological parameters due to the presence of phytochemicals such as phenol, resins, saponins, sterols, tannis and terpenes in the triherbal formula. Therefore, it has potential to induce haematotoxicity hence consumption of high concentrations should be discouraged.

pharmacology and toxicology↗

bioRxiv2020

Potential Hematotoxicity and Genotoxicity of Multi-Herbal Formulations in Albino Mice (Mus musculus)

The current increase in the use of multi-herbal remedies coupled with loose regulation on public access to these products underscore research efforts to evaluate their biochemical effect, noting that many of the herbal medicines lack scientific evidence to support their medicinal claims. Objective: We therefore investigated the potential genotoxicity and hematotoxicity of commonly consumed multi-herbal formulations (YoyoBitters, Ogidiga and BabyOku) in Lagos, Nigeria, in experimental mice. Methods: Fifty (50) adult female albino mice were randomly selected and distributed into 5 groups of 10 mice each. Two mL/kg body weight of distilled water were orally administered to the control groups while BabyOku, YoyoBitters and Ogidiga herbal formulations were administered to the experimental groups at doses of 2 mL/kg body weights. Results: A dose- and tissue-dependent increase in induction of apoptotic DNA fragmentation was observed in the triherbal groups relative to control groups. Also, an increase in micronucleated polychromatic erythrocytes was formed in a dose-dependent manner in the multi-herbal groups when compared with the control groups. Conclusion: From our findings, multi-herbal formulations may possess hematotoxic and genotoxic potentials in mice.

cell biology↗

bioRxiv2020

Underpinning wheat physiological and molecular responses to co-occurring iron and phosphate deficiency stress

Iron (Fe) and phosphorus (P) are the essential mineral nutrient for plant growth and development. However, the molecular interaction of the Fe and P pathways in crops remained largely obscure. In this study, we provide a comprehensive physiological and molecular analysis of hexaploid wheat response to single (Fe, P) and its combinatorial deficiencies. Our data showed that inhibition of the primary root growth occurs in response to Fe deficiency; however, growth was rescued when combinatorial deficiencies occurred. Analysis of RNAseq revealed that distinct molecular rearrangements during combined deficiencies with predominance for genes related to metabolic pathways and secondary metabolite biosynthesis primarily include genes for UDP-glycosyltransferase, cytochrome-P450s, and glutathione metabolism. Interestingly, the Fe-responsive cis-regulatory elements in the roots in Fe stress conditions were enriched compared to the combined stress. Our metabolome data also revealed the accumulation of distinct metabolites such as amino-isobutyric acid, arabinonic acid, and aconitic acid in the combined stress environment. Overall, these results are essential in developing new strategies to improve the resilience of crops in limited nutrients. HIGHLIGHTSO_LIThis study was performed to understand the molecular changes occurring during the interaction of Phosphorus (P) and Iron (Fe) in hexaploid wheat roots. C_LIO_LIP and Fe show cross-talk as Fe deficiency-induced phenotype that was restored by the withdrawal of P. C_LIO_LIA total of 2780 differentially expressed genes were identified in the roots with the combined -Fe-P deficiencies with predominance for UDP-glycosyltransferases, cytochrome-450 and glutathione-S-transferases transcripts. C_LIO_LIThe metabolomic changes identified the importance of amino-isobutyric acid, arabinonic acid and aconitic acid during dual deficiency C_LIO_LIThis work provides a comprehensive insight to understand the molecular rearrangements occurring in wheat roots during Fe and P interaction. C_LI

plant biology↗

bioRxiv2019

Evolutionarily ancient BAH-PHD protein mediates Polycomb silencing

Methylation of histone H3 lysine 27 (H3K27) is widely recognized as a transcriptionally repressive chromatin modification but the mechanism of repression remains unclear. We devised and implemented a forward genetic scheme to identify factors required for H3K27 methylation-mediated silencing in the filamentous fungus Neurospora crassa and identified a bromo-adjacent homology (BAH)-plant homeodomain (PHD)-containing protein, EPR-1 (Effector of Polycomb Repression 1; NCU07505). EPR-1 associates with H3K27 methylation in vivo and in vitro, and loss of EPR-1 de-represses H3K27-methylated genes without loss of H3K27 methylation. EPR-1 is not fungal-specific; orthologs of EPR-1 are present in a diverse array of eukaryotic lineages, suggesting an ancestral EPR-1 was a component of a primitive Polycomb repression pathway. SignificancePolycomb group (PcG) proteins are employed by a wide variety of eukaryotes for the maintenance of gene repression. Polycomb repressive complex 2 (PRC2), a multimeric complex of PcG proteins, catalyzes the methylation of histone H3 lysine 27 (H3K27). In the filamentous fungus, Neurospora crassa, H3K27 methylation represses scores of genes, despite the absence of canonical H3K27 methylation effectors that are present in plants and animals. We report the identification and characterization of an H3K27 methylation effector, EPR-1, in N. crassa and demonstrate its widespread presence and early eukaryotic origins with phylogenetic analyses. These findings indicate that an ancient EPR-1 may have been part of a nascent Polycomb repression system in eukaryotes.

molecular biology↗