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The identification of genes that confer either extension of life span or accelerate age-related decline was a step forward in understanding the mechanisms of aging and revealed that it is partially controlled by genetics and transcriptional programs. Here, we discovered that the human DNA sequence C16ORF70 encodes a protein, named MYTHO (macroautophagy and youth optimizer), which controls life span and health span. MYTHO protein is conserved from Caenorhabditis elegans to humans and its mRNA was upregulated in aged mice and elderly people. Deletion of the orthologous myt-1 gene in C. elegans dramatically shortened life span and decreased animal survival upon exposure to oxidative stress. Mechanistically, MYTHO is required for autophagy likely because it acts as a scaffold that binds WIPI2 and BCAS3 to recruit and assemble the conjugation system at the phagophore, the nascent autophagosome. We conclude that MYTHO is a transcriptionally regulated initiator of autophagy that is central in promoting stress resistance and healthy aging., Introduction In nature, organisms are continuously exposed to environmental stresses that challenge their survival. The species that quickly and efficiently adapt to hostile conditions are positively selected. This response is [...]

Molecular profiling of clear cell renal cell carcinoma (ccRCC) tumors of patients in a clinical trial has identified distinct transcriptomic signatures with predictive value, yet data in non-clear cell variants (nccRCC) are lacking. We examined the transcriptional profiles of RCC tumors representing key molecular pathways, from a multi-institutional, real- world patient cohort, including ccRCC and centrally reviewed nccRCC samples. ccRCC had increased angiogenesis signature scores compared with the heterogeneous group of nccRCC tumors, while cell cycle, fatty acid oxidation/AMPK signaling, and fatty acid synthesis/pentose phosphate signature scores were increased in one or more nccRCC subtypes. Among both ccRCC and nccRCC tumors, T effector scores statistically correlated with increased immune cell infiltration and were more commonly associated with immunotherapy-related markers ([PD- L1.sup.+]/[TMB.sup.hi]/[MSI.sup.hi]). In conclusion, this study provides evidence of differential gene transcriptional profiles among ccRCC versus nccRCC tumors, providing insights for optimizing personalized and histology-specific therapeutic strategies for patients with advanced RCC., Introduction Renal cell carcinoma (RCC) is a common cancer among men and women in the United States, with an estimated 81,800 new cases and 14,890 deaths expected in 2023 (1). [...]

One critical mechanism through which prostate cancer (PCa) adapts to treatments targeting androgen receptor (AR) signaling is the emergence of ligand-binding domain-truncated and constitutively active AR splice variants, particularly AR-V7. While AR-V7 has been intensively studied, its ability to activate distinct biological functions compared with the full- length AR (AR-FL), and its role in regulating the metastatic progression of castration- resistant PCa (CRPC), remain unclear. Our study found that, under castrated conditions, AR-V7 strongly induced osteoblastic bone lesions, a response not observed with ARFL overexpression. Through combined ChIP-seq, ATAC-seq, and RNA-seq analyses, we demonstrated that AR-V7 uniquely accesses the androgen-responsive elements in compact chromatin regions, activating a distinct transcription program. This program was highly enriched for genes involved in epithelial-mesenchymal transition and metastasis. Notably, we discovered that SOX9, a critical metastasis driver gene, was a direct target and downstream effector of AR-V7. Its protein expression was dramatically upregulated in AR-V7-induced bone lesions. Moreover, we found that Ser81 phosphorylation enhanced AR-V7's pro-metastasis function by selectively altering its specific transcription program. Blocking this phosphorylation with CDK9 inhibitors impaired the AR-V7-mediated metastasis program. Overall, our study has provided molecular insights into the role of AR splice variants in driving the metastatic progression of CRPC., Introduction The androgen receptor (AR) is critical in driving prostate cancer (PCa) development, with androgen deprivation therapy (ADT) being the standard treatment for PCa patients. Although initial responses are generally [...]

Uncontrolled accumulation of extracellular matrix leads to tissue fibrosis and loss of organ function. We previously demonstrated in vitro that the DNA/RNA-binding protein fused in sarcoma (FUS) promotes fibrotic responses by translocating to the nucleus, where it initiates collagen gene transcription. However, it is still not known whether FUS is profibrotic in vivo and whether preventing its nuclear translocation might inhibit development of fibrosis following injury. We now demonstrate that levels of nuclear FUS are significantly increased in mouse models of kidney and liver fibrosis. To evaluate the direct role of FUS nuclear translocation in fibrosis, we used mice that carry a mutation in the FUS nuclear localization sequence (FUSR521G) and the cell-penetrating peptide CP-FUS-NLS that we previously showed inhibits FUS nuclear translocation in vitro. We provide evidence that FUSR521G mice or CP-FUS-NLS-treated mice showed reduced nuclear FUS and fibrosis following injury. Finally, differential gene expression analysis and immunohistochemistry of tissues from individuals with focal segmental glomerulosclerosis or nonalcoholic steatohepatitis revealed significant upregulation of FUS and/or collagen genes and FUS protein nuclear localization in diseased organs. These results demonstrate that injury-induced nuclear translocation of FUS contributes to fibrosis and highlight CP-FUS-NLS as a promising therapeutic option for organ fibrosis., Introduction Organ fibrosis is characterized by excessive deposition of extracellular matrix (ECM) components (mainly collagen) within an injured organ that leads to the disruption of normal tissue architecture and loss [...]

* Context.--Diagnostic testing for SARS-CoV-2 in symptomatic and asymptomatic children remains integral to care, particularly for supporting return to and attendance in schools. The concordance of SARS-CoV-2 detection in children, using various specimen types, has not been widely studied. Objective.--To compare 3 sample types for SARS-CoV-2 polymerase chain reaction (PCR) testing in children, collected and tested at a single facility. Design.--We prospectively recruited 142 symptomatic and asymptomatic children/young adults into a sample comparison study performed in a single health care system. Each child provided self-collected saliva, and a trained health care provider collected a mid-turbinate nasal swab and nasopharyngeal (NP) swab. Specimens were assayed within 24 hours of collection by using reverse transcription-polymerase chain reaction (RT-PCR) to detect SARS-CoV-2 on a single testing platform. Results.--Concurrently collected saliva and mid-turbinate swabs had greater than 95% positive agreement with NP swabs when obtained within 10 days of symptom onset. Positive agreement of saliva and mid-turbinate samples collected from children with symptom onset >10 days prior, or without symptoms, was 82% compared to NP swab samples. Cycle threshold (Ct) values for mid-turbinate nasal samples more closely correlated with Ct values from NP samples than from saliva samples. Conclusions.--These findings suggest that all 3 sample types from children are useful for SARS-CoV-2 diagnostic testing by RT-PCR, and that concordance is greatest when the child has had symptoms of COVID-19 within the past 10 days. This study provides scientific justification for using sample types other than the NP swab for SARS-CoV-2 testing in pediatric populations. (Arch Pathol Lab Med. 2022;146:1056-1061; doi: 10.5858/arpa.2021-0625-SA), A pandemic provides a unique setting upon which the basic tenets of laboratory medicine are challenged. Specimen collection for SARS-CoV-2 is one such example, for which validation studies, which are [...]

A method for the quantitative determination of mRNA of TEM-type serine beta-lactamases in bacteria resistant to beta-lactam antibiotics has been developed. The method includes several stages: the isolation of a total RNA fraction from a bacterial culture and the production of the beta-lactamase target DNA in sequential reverse transcription and polymerase chain reaction with the incorporation of a biotin label, and the hybridization of the target DNA on colorimetric biochips. Sample preparation conditions were optimized to increase the yield of the analyzed target DNA. A calibration curve for determining the amount of mRNA was constructed using a standard sample of beta-lactamase TEM-1 mRNA obtained by transcription in vitro. The advantage of using a standard sample corresponding to the full-length bla.sub.TEM-1 gene is that it passes through all the stages of analysis in parallel with the test samples with the same efficiency. The detection limit for TEM-1 beta-lactamase mRNA was 0.40 ± 0.05 amol/mL; the range of determined concentrations was from 1.0 amol/mL to 2000 fmol/mL, and the relative standard deviation did not exceed 12%. The duration of analysis after the production of a bacterial culture was about 7 h. The developed method can be used to study the conditions for the expression of beta-lactamase genes in bacteria resistant to antimicrobial drugs., Author(s): M. Yu. Rubtsova [sup.1], A. A. Filippova [sup.1], N. K. Fursova [sup.2], V. G. Grigorenko [sup.1], G. V. Presnova [sup.1], M. M. Ulyashova [sup.1], A. M. Egorov [sup.1] Author [...]

Stability of the epigenetic landscape underpins maintenance of the cell-type-specific transcriptional profile. As one of the main repressive epigenetic systems, DNA methylation has been shown to be important for long-term gene silencing; its loss leads to ectopic and aberrant transcription in differentiated cells and cancer.sup.1. The developing mouse germ line endures global changes in DNA methylation in the absence of widespread transcriptional activation. Here, using an ultra-low-input native chromatin immunoprecipitation approach, we show that following DNA demethylation the gonadal primordial germ cells undergo remodelling of repressive histone modifications, resulting in a sex-specific signature in mice. We further demonstrate that Polycomb has a central role in transcriptional control in the newly hypomethylated germline genome as the genetic loss of Ezh2 leads to aberrant transcriptional activation, retrotransposon derepression and dramatic loss of developing female germ cells. This sex-specific effect of Ezh2 deletion is explained by the distinct landscape of repressive modifications observed in male and female germ cells. Overall, our study provides insight into the dynamic interplay between repressive chromatin modifications in the context of a developmental reprogramming system. Following global DNA demethylation, mouse gonadal primordial germ cells undergo remodelling of repressive chromatin modifications, resulting in a sex-specific signature that is required to safeguard the transcriptional program., Author(s): Tien-Chi Huang [sup.1] [sup.2] , Yi-Fang Wang [sup.1] , Eric Vazquez-Ferrer [sup.1] [sup.2] , Ina Theofel [sup.1] [sup.2] , Cristina E. Requena [sup.1] [sup.2] , Courtney W. Hanna [sup.3] [...]

The repair of DNA double-strand breaks (DSBs) is essential for safeguarding genome integrity. When a DSB forms, the PI3K-related ATM kinase rapidly triggers the establishment of megabase-sized, chromatin domains decorated with phosphorylated histone H2AX ([gamma]H2AX), which act as seeds for the formation of DNA-damage response foci.sup.1. It is unclear how these foci are rapidly assembled to establish a 'repair-prone' environment within the nucleus. Topologically associating domains are a key feature of 3D genome organization that compartmentalize transcription and replication, but little is known about their contribution to DNA repair processes.sup.2,3. Here we show that topologically associating domains are functional units of the DNA damage response, and are instrumental for the correct establishment of [gamma]H2AX-53BP1 chromatin domains in a manner that involves one-sided cohesin-mediated loop extrusion on both sides of the DSB. We propose a model in which H2AX-containing nucleosomes are rapidly phosphorylated as they actively pass by DSB-anchored cohesin. Our work highlights the importance of chromosome conformation in the maintenance of genome integrity and demonstrates the establishment of a chromatin modification by loop extrusion. During the repair of double-stranded DNA breaks, cohesin mediates the extrusion of loops of DNA along which phosphorylated H2AX spreads to establish a repair zone., Author(s): Coline Arnould [sup.1] , Vincent Rocher [sup.1] , Anne-Laure Finoux [sup.1] , Thomas Clouaire [sup.1] , Kevin Li [sup.2] , Felix Zhou [sup.2] , Pierre Caron [sup.1] , Philippe. [...]

The intensive application of inorganic nitrogen underlies marked increases in crop production, but imposes detrimental effects on ecosystems.sup.1,2: it is therefore crucial for future sustainable agriculture to improve the nitrogen-use efficiency of crop plants. Here we report the genetic basis of nitrogen-use efficiency associated with adaptation to local soils in rice (Oryza sativa L.). Using a panel of diverse rice germplasm collected from different ecogeographical regions, we performed a genome-wide association study on the tillering response to nitrogen--the trait that is most closely correlated with nitrogen-use efficiency in rice--and identified OsTCP19 as a modulator of this tillering response through its transcriptional response to nitrogen and its targeting to the tiller-promoting gene DWARF AND LOW-TILLERING (DLT).sup.3,4. A 29-bp insertion and/or deletion in the OsTCP19 promoter confers a differential transcriptional response and variation in the tillering response to nitrogen among rice varieties. The allele of OsTCP19 associated with a high tillering response to nitrogen is prevalent in wild rice populations, but has largely been lost in modern cultivars: this loss correlates with increased local soil nitrogen content, which suggests that it might have contributed to geographical adaptation in rice. Introgression of the allele associated with a high tillering response into modern rice cultivars boosts grain yield and nitrogen-use efficiency under low or moderate levels of nitrogen, which demonstrates substantial potential for rice breeding and the amelioration of negative environment effects by reducing the application of nitrogen to crops. OsTCP19 is a modulator of the tillering response to nitrogen in rice, and introgression of an allele of OsTCP19 associated with a high tillering response into modern rice cultivars markedly improves their nitrogen-use efficiency., Author(s): Yongqiang Liu [sup.1] [sup.2] , Hongru Wang [sup.1] , Zhimin Jiang [sup.1] , Wei Wang [sup.1] , Ruineng Xu [sup.3] [sup.4] , Qihui Wang [sup.5] , Zhihua Zhang [sup.1] [...]

Introduction Global influenza virus surveillance has been conducted through WHO Global Influenza Surveillance and Response System (GISRS) for over 65 years. (1) Currently, over 147 institutions are recognized by WHO [...]

Single-cell RNA sequencing of embryos can resolve the transcriptional landscape of development at unprecedented resolution. To date, single-cell RNA-sequencing studies of mammalian embryos have focused exclusively on eutherian species. Analysis of mammalian outgroups has the potential to identify deeply conserved lineage specification and pluripotency factors, and can extend our understanding of X dosage compensation. Metatherian (marsupial) mammals diverged from eutherians around 160 million years ago. They exhibit distinctive developmental features, including late implantation.sup.1 and imprinted X chromosome inactivation.sup.2, which is associated with expression of the XIST-like noncoding RNA RSX.sup.3. Here we perform a single-cell RNA-sequencing analysis of embryogenesis and X chromosome inactivation in a marsupial, the grey short-tailed opossum (Monodelphis domestica). We resolve the developmental trajectory and transcriptional signatures of the epiblast, primitive endoderm and trophectoderm, and identify deeply conserved lineage-specific markers that pre-date the eutherian-marsupial divergence. RSX coating and inactivation of the X chromosome occurs early and rapidly. This observation supports the hypothesis that--in organisms with early X chromosome inactivation--imprinted X chromosome inactivation prevents biallelic X silencing. We identify XSR, an RSX antisense transcript expressed from the active X chromosome, as a candidate for the regulator of imprinted X chromosome inactivation. Our datasets provide insights into the evolution of mammalian embryogenesis and X dosage compensation. Single-cell RNA-sequencing analysis of embryogenesis and X chromosome inactivation in the opossum (Monodelphis domestica) resolves the developmental trajectory of a marsupial, and sheds light on the evolution of embryogenesis in mammals., Author(s): Shantha K. Mahadevaiah [sup.1] , Mahesh N. Sangrithi [sup.2] [sup.3] , Takayuki Hirota [sup.1] , James M. A. Turner [sup.1] Author Affiliations: (1) Sex Chromosome Biology Laboratory, The Francis [...]

During mammalian embryogenesis, differential gene expression gradually builds the identity and complexity of each tissue and organ system.sup.1. Here we systematically quantified mouse polyA-RNA from day 10.5 of embryonic development to birth, sampling 17 tissues and organs. The resulting developmental transcriptome is globally structured by dynamic cytodifferentiation, body-axis and cell-proliferation gene sets that were further characterized by the transcription factor motif codes of their promoters. We decomposed the tissue-level transcriptome using single-cell RNA-seq (sequencing of RNA reverse transcribed into cDNA) and found that neurogenesis and haematopoiesis dominate at both the gene and cellular levels, jointly accounting for one-third of differential gene expression and more than 40% of identified cell types. By integrating promoter sequence motifs with companion ENCODE epigenomic profiles, we identified a prominent promoter de-repression mechanism in neuronal expression clusters that was attributable to known and novel repressors. Focusing on the developing limb, single-cell RNA data identified 25 candidate cell types that included progenitor and differentiating states with computationally inferred lineage relationships. We extracted cell-type transcription factor networks and complementary sets of candidate enhancer elements by using single-cell RNA-seq to decompose integrative cis-element (IDEAS) models that were derived from whole-tissue epigenome chromatin data. These ENCODE reference data, computed network components and IDEAS chromatin segmentations are companion resources to the matching epigenomic developmental matrix, and are available for researchers to further mine and integrate. RNA expression is quantified at a tissue level in seventeen mouse tissues across embryonic development, and at the single-cell level in the developing limb., Author(s): Peng He [sup.1] [sup.10] , Brian A. Williams [sup.1] , Diane Trout [sup.1] , Georgi K. Marinov [sup.2] , Henry Amrhein [sup.1] , Libera Berghella [sup.1] , Say-Tar Goh [...]

Complex organisms can rapidly induce select genes in response to diverse environmental cues. This regulation occurs in the context of large genomes condensed by histone proteins into chromatin. The sensing of pathogens by macrophages engages conserved signalling pathways and transcription factors to coordinate the induction of inflammatory genes.sup.1-3. Enriched integration of histone H3.3, the ancestral histone H3 variant, is a general feature of dynamically regulated chromatin and transcription.sup.4-7. However, how chromatin is regulated at induced genes, and what features of H3.3 might enable rapid and high-level transcription, are unknown. The amino terminus of H3.3 contains a unique serine residue (Ser31) that is absent in 'canonical' H3.1 and H3.2. Here we show that this residue, H3.3S31, is phosphorylated (H3.3S31ph) in a stimulation-dependent manner along rapidly induced genes in mouse macrophages. This selective mark of stimulation-responsive genes directly engages the histone methyltransferase SETD2, a component of the active transcription machinery, and 'ejects' the elongation corepressor ZMYND11.sup.8,9. We propose that features of H3.3 at stimulation-induced genes, including H3.3S31ph, provide preferential access to the transcription apparatus. Our results indicate dedicated mechanisms that enable rapid transcription involving the histone variant H3.3, its phosphorylation, and both the recruitment and the ejection of chromatin regulators. The histone variant H3.3 is phosphorylated at Ser31 in induced genes, and this selective mark stimulates the histone methyltransferase SETD2 and ejects the ZMYND11 repressor, thus revealing a role for histone phosphorylation in amplifying de novo transcription., Author(s): Anja Armache [sup.1] [sup.2] , Shuang Yang [sup.3] , Alexia Martínez de Paz [sup.1] , Lexi E. Robbins [sup.1] , Ceyda Durmaz [sup.1] , Jin Q. Cheong [sup.1] , [...]

Grafts of spinal-cord-derived neural progenitor cells (NPCs) enable the robust regeneration of corticospinal axons and restore forelimb function after spinal cord injury.sup.1; however, the molecular mechanisms that underlie this regeneration are unknown. Here we perform translational profiling specifically of corticospinal tract (CST) motor neurons in mice, to identify their 'regenerative transcriptome' after spinal cord injury and NPC grafting. Notably, both injury alone and injury combined with NPC grafts elicit virtually identical early transcriptomic responses in host CST neurons. However, in mice with injury alone this regenerative transcriptome is downregulated after two weeks, whereas in NPC-grafted mice this transcriptome is sustained. The regenerative transcriptome represents a reversion to an embryonic transcriptional state of the CST neuron. The huntingtin gene (Htt) is a central hub in the regeneration transcriptome; deletion of Htt significantly attenuates regeneration, which shows that Htt has a key role in neural plasticity after injury. In mouse models of central nervous system injury, Htt is shown to be a key component of the regulatory program associated with reversion of the neuronal transcriptome to a less-mature state., Author(s): Gunnar H. D. Poplawski [sup.1] , Riki Kawaguchi [sup.2] [sup.3] , Erna Van Niekerk [sup.1] , Paul Lu [sup.1] [sup.4] , Neil Mehta [sup.1] , Philip Canete [sup.1] , [...]

The chromatin-remodelling complex SWI/SNF is highly conserved and has critical roles in various cellular processes, including transcription and DNA-damage repair.sup.1,2. It hydrolyses ATP to remodel chromatin structure by sliding and evicting histone octamers.sup.3-8, creating DNA regions that become accessible to other essential factors. However, our mechanistic understanding of the remodelling activity is hindered by the lack of a high-resolution structure of complexes from this family. Here we report the cryo-electron microscopy structure of Saccharomyces cerevisiae SWI/SNF bound to a nucleosome, at near-atomic resolution. In the structure, the actin-related protein (Arp) module is sandwiched between the ATPase and the rest of the complex, with the Snf2 helicase-SANT associated (HSA) domain connecting all modules. The body contains an assembly scaffold composed of conserved subunits Snf12 (also known as SMARCD or BAF60), Snf5 (also known as SMARCB1, BAF47 or INI1) and an asymmetric dimer of Swi3 (also known as SMARCC, BAF155 or BAF170). Another conserved subunit, Swi1 (also known as ARID1 or BAF250), resides in the core of SWI/SNF, acting as a molecular hub. We also observed interactions between Snf5 and the histones at the acidic patch, which could serve as an anchor during active DNA translocation. Our structure enables us to map and rationalize a subset of cancer-related mutations in the human SWI/SNF complex and to propose a model for how SWI/SNF recognizes and remodels the +1 nucleosome to generate nucleosome-depleted regions during gene activation.sup.9. The cryo-electron microscopy structure of the yeast SWI/SNF complex bound to a nucleosome substrate provides insights into the chromatin-remodelling function of this family of protein complexes and suggests mechanisms by which the mutated proteins may cause cancer., Author(s): Yan Han [sup.1] , Alexis A Reyes [sup.1] [sup.2] , Sara Malik [sup.1] , Yuan He [sup.1] [sup.2] [sup.3] [sup.4] Author Affiliations: (1) Department of Molecular Biosciences, Northwestern University, [...]

Xist represents a paradigm for the function of long non-coding RNA in epigenetic regulation, although how it mediates X-chromosome inactivation (XCI) remains largely unexplained. Several proteins that bind to Xist RNA have recently been identified, including the transcriptional repressor SPEN.sup.1-3, the loss of which has been associated with deficient XCI at multiple loci.sup.2-6. Here we show in mice that SPEN is a key orchestrator of XCI in vivo and we elucidate its mechanism of action. We show that SPEN is essential for initiating gene silencing on the X chromosome in preimplantation mouse embryos and in embryonic stem cells. SPEN is dispensable for maintenance of XCI in neural progenitors, although it significantly decreases the expression of genes that escape XCI. We show that SPEN is immediately recruited to the X chromosome upon the upregulation of Xist, and is targeted to enhancers and promoters of active genes. SPEN rapidly disengages from chromatin upon gene silencing, suggesting that active transcription is required to tether SPEN to chromatin. We define the SPOC domain as a major effector of the gene-silencing function of SPEN, and show that tethering SPOC to Xist RNA is sufficient to mediate gene silencing. We identify the protein partners of SPOC, including NCoR/SMRT, the m.sup.6A RNA methylation machinery, the NuRD complex, RNA polymerase II and factors involved in the regulation of transcription initiation and elongation. We propose that SPEN acts as a molecular integrator for the initiation of XCI, bridging Xist RNA with the transcription machinery--as well as with nucleosome remodellers and histone deacetylases--at active enhancers and promoters. The transcriptional repressor SPEN bridges the non-coding RNA Xist to transcription machinery, histone deacetylases and chromatin remodelling factors to initiate X-chromosome inactivation., Author(s): François Dossin [sup.1] , Inês Pinheiro [sup.2] , Jan J. Zylicz [sup.2] [sup.3] , Julia Roensch [sup.2] , Samuel Collombet [sup.1] , Agnès Le Saux [sup.2] , Tomasz Chelmicki [...]

Arsenic is a widespread toxic metalloid that is classified as a class I carcinogen known to cause adverse health effects in humans. In the present study, we investigated arsenic accumulation potential and comparative gene expression in Indian mustard. The amount of arsenic accumulated in shoots varied in the range of 15.99-1138.70 mg/kg on a dry weight basis among five cultivars. Comparative expression analysis revealed 10 870 significantly differentially expressed genes mostly belonging to response to stress, metabolic processes, signal transduction, transporter activity, and transcription regulator activity to be up-regulated, while most of the genes involved in photosynthesis, developmental processes, and cell growth were found to be down-regulated in arsenic-treated tissues. Further, pathway analysis using the KEGG Automated Annotation server (KAAS) revealed a large-scale reprogramming of genes involved in genetic and environmental information processing pathways. Top pathways with maximum KEGG orthology hits included carbon metabolism (2.5%), biosynthesis of amino acids (2.1%), plant hormone signal transduction (1.4%), and glutathione metabolism (0.6%). A transcriptomic investigation to understand the arsenic accumulation and detoxification in Indian mustard will not only help to improve its phytoremediation efficiency but also add to the control measures required to check bioaccumulation of arsenic in the food chain. Key words: arsenic, Brassica juncea, phytoremediation, transcriptome, pathway analysis. L'arsenique est un metalloïde toxique repandu qui est classifie comme un cancerogene de classe I connu pour entraîner des effets nefastes sur la sante des humains. Dans le present travail, les auteurs ont etudie le potentiel d'accumulation de l'arsenique et l'expression differentielle chez la moutarde brune. La quantite d'arsenique accumulee dans les tiges variait entre 15,99 et 1138,70 mg/kg sur la base de la matiere seche parmi cinq cultivars. Une analyse comparative de l'expression genique a permis d'identifier 10 870 genes presentant une expression differentielle significative. La plupart de ceux qui etait exprimes a la hausse suite a un traitement a l'arsenique etaient annotes comme etant lies a la reponse aux stress, a des processus metaboliques, a la transduction de signaux, a divers types de transport ainsi qu'a des facteurs de transcription. Ceux exprimes moins abondamment etaient annotes comme etant associes a la photosynthese, aux processus developpementaux et a la croissance cellulaire. De plus, une analyse de sentiers a l'aide du <> (KAAS) a revele une reprogrammation globale des genes impliques dans la reponse aux informations genetiques et environnementales. Les principaux sentiers presentant le plus d'orthologues KEGG incluaient le metabolisme du carbone (2,5 %), la synthese des acides amines (2,1 %), la transduction des signaux hormonaux (1,4 %) et le metabolisme du glutathion (0,6 %). Une analyse transcriptomique visant a comprendre l'accumulation et la detoxication de l'arsenique chez la moutarde brune permettra non seulement d'ameliorer son efficacite en matiere de phytoremediation, mais pourra aussi contribuer aux mesures de contrôle visant a etablir la bioaccumulation de l'arsenique dans la chaîne alimentaire. [Traduit par la Redaction] Mots-cles : arsenique, Brassica juncea, phytoremediation, transcriptome, analyse des sentiers., Introduction Arsenic is the 20th most abundant element and a toxic metalloid that is present in the Earth's crust. Its average concentration is 2-5 mg/kg (Moore 1991). Because of its [...]