'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Fri, 20 Jan 2017 19:31:15 PST Fri, 20 Jan 2017 19:31:15 PST jirtle@radonc.duke.edu james001@jirtle.com Host-microbiota interactions: epigenomic regulation. Woo V, Alenghat T
Curr Opin Immunol (Jan 2017)

The coevolution of mammalian hosts and their commensal microbiota has led to the development of complex symbiotic relationships between resident microbes and mammalian cells. Epigenomic modifications enable host cells to alter gene expression without modifying the genetic code, and therefore represent potent mechanisms by which mammalian cells can transcriptionally respond, transiently or stably, to environmental cues. Advances in genome-wide approaches are accelerating our appreciation of microbial influences on host physiology, and increasing evidence highlights that epigenomics represent a level of regulation by which the host integrates and responds to microbial signals. In particular, bacterial-derived short chain fatty acids have emerged as one clear link between how the microbiota intersects with host epigenomic pathways. Here we review recent findings describing crosstalk between the microbiota and epigenomic pathways in multiple mammalian cell populations. Further, we discuss interesting links that suggest that the scope of our understanding of epigenomic regulation in the host-microbiota relationship is still in its infancy.]]>
Thu, 19 Jan 2017 00:00:00 PST
Imprinted genes and the regulation of placental endocrine function: Pregnancy and beyond. John RM
Placenta (Jan 2017)

Genomic imprinting is an epigenetic process responsible for the monoallelic expression of a subset of genes in mammals. Imprinted genes have been demonstrated to play important functions prenatally regulating fetal growth and placental development with some functions persisting beyond pregnancy to influence both metabolism and behaviour in adults. This review focuses on the function of imprinted genes in regulating placental hormones, and the probability that these functions manifest their impact beyond pregnancy.]]>
Tue, 17 Jan 2017 00:00:00 PST
Single-Cell Multiomics: Multiple Measurements from Single Cells. Macaulay IC, Ponting CP, Voet T
Trends Genet (Jan 2017)

Single-cell sequencing provides information that is not confounded by genotypic or phenotypic heterogeneity of bulk samples. Sequencing of one molecular type (RNA, methylated DNA or open chromatin) in a single cell, furthermore, provides insights into the cell's phenotype and links to its genotype. Nevertheless, only by taking measurements of these phenotypes and genotypes from the same single cells can such inferences be made unambiguously. In this review, we survey the first experimental approaches that assay, in parallel, multiple molecular types from the same single cell, before considering the challenges and opportunities afforded by these and future technologies.]]>
Mon, 16 Jan 2017 00:00:00 PST
DNA methylation of imprinted loci of autosomal chromosomes and IGF2 is not affected in Parkinson's disease patients' peripheral blood mononuclear cells. Kaut O, Sharma A, Schmitt I, Wüllner U
Neurol Res (Jan 2017)

 Genomic imprinting is an epigenetic phenomenon that results in differential expression of alleles, depending on their parental origin. The functional significance of DNA methylation in genomic imprinting has been widely investigated, and to date, approximately 100 imprinted genes have been identified in humans.]]>
Fri, 13 Jan 2017 00:00:00 PST
Chromatin Dynamics Regulate Mesenchymal Stem Cell Lineage Specification and Differentiation to Osteogenesis. Wu H, Gordon JA, Whitfield TW, Tai PW, van Wijnen AJ, Stein JL, Stein GS, Lian JB
Biochim Biophys Acta (Jan 2017)

Multipotent mesenchymal stromal cells (MSCs) are critical for regeneration of multiple tissues. Epigenetic mechanisms are fundamental regulators of lineage specification and cell fate, and as such, we addressed the question of which epigenetic modifications characterize the transition of nascent MSCs to a tissue specific MSC-derived phenotype. By profiling the temporal changes of seven histone marks correlated to gene expression during proliferation, early commitment, matrix deposition, and mineralization stages, we identified distinct epigenetic mechanisms that regulate transcriptional programs necessary for tissue-specific phenotype development. Patterns of stage-specific enrichment of histone modifications revealed distinct modes of repression and activation of gene expression that would not be detected using single endpoint analysis. We discovered that at commitment, H3K27me3 is removed from genes that are upregulated and is not acquired on downregulated genes. Additionally, we found that the absence of H3K4me3 modification at promoters defined a subset of osteoblast-specific upregulated genes, indicating acquisition of acetyl modifications drive activation of these genes. Significantly, loss or gain of H3K36me3 was the primary predictor of dynamic changes in temporal gene expression. Using unsupervised pattern discovery analysis the signature of osteogenic-related histone modifications identified novel functional cis regulatory modules associated with enhancer regions that control tissue-specific genes. Our work provides a cornerstone to understand the epigenetic regulation of transcriptional programs that are important for MSC lineage commitment and lineage, as well as insights to facilitate MSC-based therapeutic interventions.]]>
Thu, 12 Jan 2017 00:00:00 PST
LncRNA/DNA binding analysis reveals losses and gains and lineage specificity of genomic imprinting in mammals. Liu H, Shang X, Zhu H
Bioinformatics (Jan 2017)

Genomic imprinting is regulated by lncRNAs and is important for embryogenesis, physiology, and behaviour in mammals. Aberrant imprinting causes diseases and disorders. Experimental studies have examined genomic imprinting primarily in humans and mice, thus leaving some fundamental issues poorly addressed. The cost of experimentally examining imprinted genes in many tissues in diverse species makes computational analysis of lncRNAs' DNA binding sites valuable.]]>
Thu, 05 Jan 2017 00:00:00 PST
Accurate Promoter and Enhancer Identification in 127 ENCODE and Roadmap Epigenomics Cell Types and Tissues by GenoSTAN. Zacher B, Michel M, Schwalb B, Cramer P, Tresch A, Gagneur J
PLoS One (2017)

Accurate maps of promoters and enhancers are required for understanding transcriptional regulation. Promoters and enhancers are usually mapped by integration of chromatin assays charting histone modifications, DNA accessibility, and transcription factor binding. However, current algorithms are limited by unrealistic data distribution assumptions. Here we propose GenoSTAN (Genomic STate ANnotation), a hidden Markov model overcoming these limitations. We map promoters and enhancers for 127 cell types and tissues from the ENCODE and Roadmap Epigenomics projects, today's largest compendium of chromatin assays. Extensive benchmarks demonstrate that GenoSTAN generally identifies promoters and enhancers with significantly higher accuracy than previous methods. Moreover, GenoSTAN-derived promoters and enhancers showed significantly higher enrichment of complex trait-associated genetic variants than current annotations. Altogether, GenoSTAN provides an easy-to-use tool to define promoters and enhancers in any system, and our annotation of human transcriptional cis-regulatory elements constitutes a rich resource for future research in biology and medicine.]]>
Thu, 05 Jan 2017 00:00:00 PST
Linking Hematopoietic Differentiation to Co-Expressed Sets of Pluripotency-Associated and Imprinted Genes and to Regulatory microRNA-Transcription Factor Motifs. Hamed M, Trumm J, Spaniol C, Sethi R, Irhimeh MR, Fuellen G, Paulsen M, Helms V
PLoS One (2017)

Maintenance of cell pluripotency, differentiation, and reprogramming are regulated by complex gene regulatory networks (GRNs) including monoallelically-expressed imprinted genes. Besides transcriptional control, epigenetic modifications and microRNAs contribute to cellular differentiation. As a model system for studying the capacity of cells to preserve their pluripotency state and the onset of differentiation and subsequent specialization, murine hematopoiesis was used and compared to embryonic stem cells (ESCs) as a control. Using published microarray data, the expression profiles of two sets of genes, pluripotent and imprinted, were compared to a third set of known hematopoietic genes. We found that more than half of the pluripotent and imprinted genes are clearly upregulated in ESCs but subsequently repressed during hematopoiesis. The remaining genes were either upregulated in hematopoietic progenitors or in differentiated blood cells. The three gene sets each consist of three similarly behaving gene groups with similar expression profiles in various lineages of the hematopoietic system as well as in ESCs. To explain this co-regulation behavior, we explored the transcriptional and post-transcriptional mechanisms of pluripotent and imprinted genes and their regulator/target miRNAs in six different hematopoietic lineages. Therewith, lineage-specific transcription factor (TF)-miRNA regulatory networks were generated and their topologies and functional impacts during hematopoiesis were analyzed. This led to the identification of TF-miRNA co-regulatory motifs, for which we validated the contribution to the cellular development of the corresponding lineage in terms of statistical significance and relevance to biological evidence. This analysis also identified key miRNAs and TFs/genes that might play important roles in the derived lineage networks. These molecular associations suggest new aspects of the cellular regulation of the onset of cellular differentiation and during hematopoiesis involving, on one hand, pluripotent genes that were previously not discussed in the context of hematopoiesis and, on the other hand, involve genes that are related to genomic imprinting. These are new links between hematopoiesis and cellular differentiation and the important field of epigenetic modifications.]]>
Wed, 04 Jan 2017 00:00:00 PST
Epigenomics alternations and dynamic transcriptional changes in responses to 5-fluorouracil stimulation reveal mechanisms of acquired drug resistance of colorectal cancer cells. Shen Y, Tong M, Liang Q, Guo Y, Sun HQ, Zheng W, Ao L, Guo Z, She F
Pharmacogenomics J (Jan 2017)

A drug-induced resistant cancer cell is different from its parent cell in transcriptional response to drug treatment. The distinct transcriptional response pattern of a drug-induced resistant cancer cell to drug treatment might be introduced by acquired DNA methylation aberration in the cell exposing to sustained drug stimulation. In this study, we performed both transcriptional and DNA methylation profiles of the HCT-8 wild-type cells (HCT-8/WT) for human colorectal cancer (CRC) and the 5-fluorouracil (5-FU)-induced resistant cells (HCT-8/5-FU) after treatment with 5-FU for 0, 24 and 48 h. Integrated analysis of transcriptional and DNA methylation profiles showed that genes with promoter hypermethylation and concordant expression silencing in the HCT-8/5-FU cells are mainly involved in pathways of pyrimidine metabolism and drug metabolism-cytochrome P450. Transcriptional analysis confirmed that genes with transcriptional differences between a drug-induced resistant cell and its parent cell after drug treatment for a certain time, rather than their primary transcriptional differences, are more likely to be involved in drug resistance. Specifically, transcriptional differences between the drug-induced resistant cells and parental cells after drug treatment for 24 h were significantly consistent with the differentially expressed genes (termed as CRG5-FU) between the tissues of nonresponders and responders of CRCs to 5-FU-based therapy and the consistence increased after drug treatment for 48 h (binomial test, P-value=1.88E-06). This study reveals a major epigenetic mechanism inducing the HCT-8/WT cells to acquire resistance to 5-FU and suggests an appropriate time interval (24-48 h) of 5-FU exposure for identifying clinically relevant drug resistance signatures from drug-induced resistant cell models.The Pharmacogenomics Journal advance online publication, 3 January 2017; doi:10.1038/tpj.2016.91.]]>
Tue, 03 Jan 2017 00:00:00 PST
Association between DNA methyltransferase gene polymorphism and Parkinson's disease. Pezzi JC, de Bem CM, da Rocha TJ, Schumacher-Schuh AF, Chaves ML, Rieder CR, Hutz MH, Fiegenbaum M, Camozzato AL
Neurosci Lett (Dec 2016)

Parkinson's disease (PD) is a common and complex neurodegenerative disorder, the second most prevalent, only behind Alzheimer's disease. Recent studies suggest that environmental factors may contribute for neurodegeneration through induction of epigenetic modifications, such as DNA methylation, that is carried out by enzymes, such as DNMT1 and DNMT3B. This present study targeted to investigate the association among DNMT1 and DNMT3B polymorphisms with PD. Five hundred and twenty-two participants (214 PD patients following UK Brain Bank criteria and 308 healthy individuals) were evaluated. DNA was obtained from whole blood and genotypes were detected by an allelic discrimination assay using TaqMan(®) MGB probes on a real-time PCR system. The polymorphisms studied were rs2162560 and rs759920 (DNMT1) and rs2424913, rs998382 and rs2424932 (DNMT3B). Was found association between DNMT3B rs2424913 in T allele carriers with PD. The presence of the T allele was associated with PD (OR=1.80, 95% CI 1.16-2.81, p=0.009). No significant difference was observed for others DNMT3B SNPs. Also, no association between PD and the control group were observed for DNMT1 polymorphisms. This is the first study addressing an association between DNMT3B polymorphism and PD. The polymorphism may play a role in the pathogenesis of PD.]]>
Mon, 02 Jan 2017 00:00:00 PST
Orbital autoimmune inflammatory disorders - Protein regional variability might explain specific lesion location. Clarke MS, Plouznikoff A, Deschenes J
Med Hypotheses (Jan 2017)

In ophthalmology, inflammatory diseases target different highly specific regions within the small confine of the orbit. Some entities even prefer a particular location or depth within the same tissue (ex. anterior, intermediate or posterior uveitides, chorioretinitides with unique topographic presentations). Though the location of a lesion strongly influences and helps us in our differential diagnosis, we still don't understand why specific anatomic sites are susceptible to a disease while other areas are spared. We postulate that regional variability in tissue protein expression can sway the immune system's capacity to trigger an autoimmune response. In addition to this site-specific quantitative and qualitative variability in potential antigen expression, we believe that other proteins implicated in the immune cascade, as well as geographic areas of relative resistance, tolerance and susceptibility, may be unequally distributed within the orbit. To illustrate our hypotheses, we review three major types of ocular myositis and describe how the extraocular muscles different embryologic origins and protein disparities might explain the fundamental clinical differences between these orbital inflammatory diseases. We hope that future differential genomics, proteinomics, epigenomics and analysis of RNA species of affected tissues, compared to their non-affected, yet microscopically similar, counterparts, will help us understand why diseases occur where they do. Hopefully, understanding these immune triggers will pave the way to new treatment options for ocular inflammatory diseases and for other auto-inflammatory conditions with a marked predilection for any given site.]]>
Sun, 25 Dec 2016 00:00:00 PST
From profiles to function in epigenomics. Stricker SH, Köferle A, Beck S
Nat Rev Genet (Jan 2017)

Myriads of epigenomic features have been comprehensively profiled in health and disease across cell types, tissues and individuals. Although current epigenomic approaches can infer function for chromatin marks through correlation, it remains challenging to establish which marks actually have causative roles in gene regulation and other processes. After revisiting how classical approaches have addressed this question in the past, we discuss the current state of epigenomic profiling and how functional information can be indirectly inferred. We also present new approaches that promise definitive functional answers, which are collectively referred to as 'epigenome editing'. In particular, we explore CRISPR-based technologies for single-locus and multi-locus manipulation. Finally, we discuss which level of function can be achieved with each approach and introduce emerging strategies for high-throughput progression from profiles to function.]]>
Mon, 21 Nov 2016 00:00:00 PST
Down-regulation of serotonin and dopamine transporter genes in individual rats expressing a gambling-prone profile: A possible role for epigenetic mechanisms. Zoratto F, Romano E, Pascale E, Pucci M, Falconi A, Dell'Osso B, Maccarrone M, Laviola G, D'Addario C, Adriani W
Neuroscience (Jan 2017)

Gambling Disorder (GD) is characterized by excessive gambling despite adverse consequences on individual functioning. In spite of some positive findings, it is difficult to draw any conclusion on the genetics of GD. Indeed, beyond DNA sequence variation, other regulatory mechanisms (like those that engage epigenetics) may explain gene alterations in this addictive disease. Wistar male rats underwent an operant task for the evaluation of individual propensity to gamble. Few rats, after having learnt to prefer nose-poking for a large over a small food reward, were sacrificed to obtain a baseline profile of gene expression at both central and peripheral levels. In the remaining rats, probability of occurrence of large-reward delivery decreased progressively to very low levels. Thus, rats were faced with temptation to "gamble", i.e. to nose-poke for a binge reward, whose delivery was omitted the majority of times. After 3weeks of testing, rats showing a clear-cut profile of either gambling proneness or aversion were selected and sacrificed after the last session. A selective down-regulation of i) serotonin transporter in prefrontal cortex, ii) tyrosine hydroxylase in ventral striatum, iii) dopamine transporter in lymphocytes was evidenced in "gambler" vs "non-gambler" rats. The exposure to such operant task (compared to home-cage alone) modulated ventrostriatal but not prefrontal genes. A consistent increase of DNA methylation, in one specific CpG site at serotonin transporter gene, was evident in prefrontal cortex of "gambler" rats. Elucidation of epigenetic changes occurring during GD progression may pave the way to the development of new therapeutic strategies through specific modulation of epigenetic factors.]]>
Fri, 28 Oct 2016 00:00:00 PDT
The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications. Vennin C, Spruyt N, Robin YM, Chassat T, Le Bourhis X, Adriaenssens E
Cancer Lett (Jan 2017)

Numerous genomic imprinting loci are regulated by long non-coding RNA (lncRNA). We have previously identified a new lncRNA at the H19/IGF2 locus transcribed in H19 antisense orientation and named 91H. This RNA is conserved among mammals. In mice, 91H regulates positively IGF2 expression from a novel promoter. However, in human the function of 91H at the H19/IGF2 locus remains largely undeciphered. Here, we observed that 91H, H19 and IGF2 are overexpressed in breast tumors. By using 91H-knockdown breast cancer cells, we demonstrated that 91H exerts oncogenic properties by promoting cell growth, migration and invasion as well as tumor growth in xenografted immunodeficient mouse model. Moreover, 91H-knockdown reduces the expression of H19 and IGF2 in breast cancer cells. By chromatin-immunoprecipitation and methylation studies, we found that 91H expression prevents histone and DNA methylation on the maternal allele at the H19/IGF2 locus. These results indicate that 91H, through epigenetic modifications, is responsible of the maintenance of H19/IGF2 genomic imprinting allowing the allele-specific expression of H19 and IGF2. Taken together, overexpression of 91H in breast cancer and 91H-induced epigenetic modifications on H19/IGF2 locus suggest that 91H may play essential role in breast cancer development. Further studies are needed to investigate their role in terms of diagnosis and therapeutic.]]>
Wed, 26 Oct 2016 00:00:00 PDT
A Synopsis of the "Influence of Epigenetics, Genetics, and Immunology" Session Part A at the 35th Annual Society of Toxicologic Pathology Symposium. Harrill AH, Moggs JG, Adkins KK, Augustin HG, Johnson RC, Leach MW
Toxicol Pathol (Jan 2017)

The overarching theme of the 2016 Society of Toxicology Pathology's Annual Symposium was "The Basis and Relevance of Variation in Toxicologic Responses." Session 4 focused on genetic variation as a potential source for variability in toxicologic responses within nonclinical toxicity studies and further explored how knowledge of genetic traits might enable targeted prospective and retrospective studies in drug development and human health risk assessment. In this session, the influence of both genetic sequence variation and epigenetic modifications on toxicologic responses and their implications for understanding risk were explored. In this overview, the presentations in this session will be summarized, with a goal of exploring the ramifications of genetic and epigenetic variability within and across species for toxicity studies and disseminating information regarding novel tools to harness this variability to advance understanding of toxicologic responses across populations.]]>
Thu, 06 Oct 2016 00:00:00 PDT
Putting DNA methylation in context: from genomes to gene expression in plants. Niederhuth CE, Schmitz RJ
Biochim Biophys Acta (Jan 2017)

Plant DNA methylation is its own language, interpreted by the cell to maintain silencing of transposons, facilitate chromatin structure, and to ensure proper expression of some genes. Just as in any language, context is important. Rather than being a simple "on-off switch", DNA methylation has a range of "meanings" dependent upon the underlying sequence and its location in the genome. Differences in the sequence context of individual sites are established, maintained, and interpreted by differing molecular pathways. Varying patterns of methylation within genes and surrounding sequences are associated with a continuous range of expression differences, from silencing to constitutive expression. These often-subtle differences have been pieced together from years of effort, but have taken off with the advent of methods for assessing methylation across entire genomes. Recognizing these patterns and identifying underlying causes is essential for understanding the function of DNA methylation and its systems-wide contribution to a range of processes in plant genomes. This article is part of a Special Issue entitled: Plant Gene Regulatory Mechanisms and Networks, edited by Dr. Erich Grotewold and Dr. Nathan Springer.]]>
Mon, 19 Sep 2016 00:00:00 PDT
Integrated Epigenomics Analysis Reveals a DNA Methylation Panel for Endometrial Cancer Detection Using Cervical Scrapings. Huang RL, Su PH, Liao YP, Wu TI, Hsu YT, Lin WY, Wang HC, Weng YC, Ou YC, Huang TH, Lai HC
Clin Cancer Res (Jan 2017)

Endometrial cancer is a common gynecologic cancer whose incidence is increasing annually worldwide. Current methods to detect endometrial cancer are unreliable and biomarkers are unsatisfactory for screening. Cervical scrapings were reported as a potential source of material for molecular testing. DNA methylation is a promising cancer biomarker, but limited use for detecting endometrial cancer.]]>
Wed, 10 Aug 2016 00:00:00 PDT
Methylation Status of H19/IGF2 Differentially Methylated Region in in vitro Human Blastocysts Donated by Healthy Couples. Derakhshan-Horeh M, Abolhassani F, Jafarpour F, Moini A, Karbalaie Kh, Hosseini SM, Ostadhosseini S, Nasr-Esfahani MH
Iran Biomed J (Jan 2017)

Imprinted genes are a unique subset of few genes that have been differentially methylated region (DMR) in a parental origin-dependent manner during gametogenesis, and these genes are highly protected during pre-implantation epigenetic reprogramming. Several studies have shown that the particular vulnerability of imprinting genes during suboptimal pre- and peri-conception micro-environments often is occurred by assisted reproduction techniques (ART). This study investigated the methylation status of H19/IGF2 DMR at high-quality expanding/expanded human blastocysts donated by healthy individuals to evaluate the risks linked to ART.]]>
Sun, 24 Jul 2016 00:00:00 PDT
Practical Guidelines for High-Resolution Epigenomic Profiling of Nucleosomal Histones in Postmortem Human Brain Tissue. Kundakovic M, Jiang Y, Kavanagh DH, Dincer A, Brown L, Pothula V, Zharovsky E, Park R, Jacobov R, Magro I, Kassim B, Wiseman J, Dang K, Sieberts SK, Roussos P, Fromer M, Harris B, Lipska BK, Peters MA, Sklar P, Akbarian S
Biol Psychiatry (Jan 2017)

The nervous system may include more than 100 residue-specific posttranslational modifications of histones forming the nucleosome core that are often regulated in cell-type-specific manner. On a genome-wide scale, some of the histone posttranslational modification landscapes show significant overlap with the genetic risk architecture for several psychiatric disorders, fueling PsychENCODE and other large-scale efforts to comprehensively map neuronal and nonneuronal epigenomes in hundreds of specimens. However, practical guidelines for efficient generation of histone chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) datasets from postmortem brains are needed.]]>
Tue, 26 Apr 2016 00:00:00 PDT
Abscisic-acid-dependent basic leucine zipper (bZIP) transcription factors in plant abiotic stress. Banerjee A, Roychoudhury A
Protoplasma (Jan 2017)

One of the major causes of significant crop loss throughout the world is the myriad of environmental stresses including drought, salinity, cold, heavy metal toxicity, and ultraviolet-B (UV-B) rays. Plants as sessile organisms have evolved various effective mechanism which enable them to withstand this plethora of stresses. Most of such regulatory mechanisms usually follow the abscisic-acid (ABA)-dependent pathway. In this review, we have primarily focussed on the basic leucine zipper (bZIP) transcription factors (TFs) activated by the ABA-mediated signalosome. Upon perception of ABA by specialized receptors, the signal is transduced via various groups of Ser/Thr kinases, which phosphorylate the bZIP TFs. Following such post-translational modification of TFs, they are activated so that they bind to specific cis-acting sequences called abscisic-acid-responsive elements (ABREs) or GC-rich coupling elements (CE), thereby influencing the expression of their target downstream genes. Several in silico techniques have been adopted so far to predict the structural features, recognize the regulatory modification sites, undergo phylogenetic analyses, and facilitate genome-wide survey of TF under multiple stresses. Current investigations on the epigenetic regulation that controls greater accessibility of the inducible regions of DNA of the target gene to the bZIP TFs exclusively under stress situations, along with the evolved stress memory responses via genomic imprinting mechanism, have been highlighted. The potentiality of overexpression of bZIP TFs, either in a homologous or in a heterologous background, in generating transgenic plants tolerant to various abiotic stressors have also been addressed by various groups. The present review will provide a coherent documentation on the functional characterization and regulation of bZIP TFs under multiple environmental stresses, with the major goal of generating multiple-stress-tolerant plant cultivars in near future.]]>
Wed, 16 Dec 2015 00:00:00 PST