'; ?> 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 Tue, 16 Oct 2018 13:12:09 EDT Tue, 16 Oct 2018 13:12:09 EDT jirtle@radonc.duke.edu james001@jirtle.com The DNA methylation landscape of glioblastoma disease progression shows extensive heterogeneity in time and space. Klughammer J, Kiesel B, Roetzer T, Fortelny N, Nemc A, Nenning KH, Furtner J, Sheffield NC, Datlinger P, Peter N, Nowosielski M, Augustin M, Mischkulnig M, Ströbel T, Alpar D, Ergüner B, Senekowitsch M, Moser P, Freyschlag CF, Kerschbaumer J, Thomé C, Grams AE, Stockhammer G, Kitzwoegerer M, Oberndorfer S, Marhold F, Weis S, Trenkler J, Buchroithner J, Pichler J, Haybaeck J, Krassnig S, Mahdy Ali K, von Campe G, Payer F, Sherif C, Preiser J, Hauser T, Winkler PA, Kleindienst W, Würtz F, Brandner-Kokalj T, Stultschnig M, Schweiger S, Dieckmann K, Preusser M, Langs G, Baumann B, Knosp E, Widhalm G, Marosi C, Hainfellner JA, Woehrer A, Bock C
Nat Med (Oct 2018)

Glioblastoma is characterized by widespread genetic and transcriptional heterogeneity, yet little is known about the role of the epigenome in glioblastoma disease progression. Here, we present genome-scale maps of DNA methylation in matched primary and recurring glioblastoma tumors, using data from a highly annotated clinical cohort that was selected through a national patient registry. We demonstrate the feasibility of DNA methylation mapping in a large set of routinely collected FFPE samples, and we validate bisulfite sequencing as a multipurpose assay that allowed us to infer a range of different genetic, epigenetic, and transcriptional characteristics of the profiled tumor samples. On the basis of these data, we identified subtle differences between primary and recurring tumors, links between DNA methylation and the tumor microenvironment, and an association of epigenetic tumor heterogeneity with patient survival. In summary, this study establishes an open resource for dissecting DNA methylation heterogeneity in a genetically diverse and heterogeneous cancer, and it demonstrates the feasibility of integrating epigenomics, radiology, and digital pathology for a national cohort, thereby leveraging existing samples and data collected as part of routine clinical practice.]]>
Wed, 31 Dec 1969 19:00:00 EST
Canine MAS1: monoallelic expression is suggestive of an imprinted gene. Nolan CM, Shiel RE, Buchan JG, O'Sullivan FM, Callanan JJ
Anim Genet (Oct 2018)

Imprinted genes are epigenetically modified in a parent-of-origin dependent manner and as a consequence are differentially expressed, with one allele typically expressed while the other is repressed. In canine, the insulin like growth factor 2 receptor gene (IGF2R) is imprinted with predominant expression of the maternally inherited allele. Because imprinted genes usually occur in clusters, we examined the allelic expression pattern of the gene encoding the canine Mas receptor (MAS1), which is located upstream of IGF2R on canine chromosome 1 and is highly conserved in mammals. In this report we describe monoallelic expression of canine MAS1 in the neonatal umbilical cord of several individuals and we identify the expressed allele as maternally inherited. These data suggest that canine MAS1 is an imprinted gene.]]>
Wed, 31 Dec 1969 19:00:00 EST
One protein to rule them all: The role of CCCTC-binding factor in shaping human genome in health and disease. Lazniewski M, Dawson WK, Rusek AM, Plewczynski D
Semin Cell Dev Biol (Oct 2018)

The eukaryotic genome, constituting several billion base pairs, must be contracted to fit within the volume of a nucleus where the diameter is on the scale of μm. The 3D structure and packing of such a long sequence cannot be left to pure chance, as DNA must be efficiently used for its primary roles as a matrix for transcription and replication. In recent years, methods like chromatin conformation capture (including 3C, 4C, Hi-C, ChIA-PET and Multi-ChIA) and optical microscopy have advanced substantially and have shed new light on how eukaryotic genomes are hierarchically organized; first into 10-nm fiber, next into DNA loops, topologically associated domains and finally into interphase or mitotic chromosomes. This knowledge has allowed us to revise our understanding regarding the mechanisms governing the process of DNA organization. Mounting experimental evidence suggests that the key element in the formation of loops is the binding of the CCCTC-binding factor (CTCF) to DNA; a protein that can be referred to as the chief organizer of the genome. However, CTCF does not work alone but in cooperation with other proteins, such as cohesin or Yin Yang 1 (YY1). In this short review, we briefly describe our current understanding of the structure of eukaryotic genomes, how they are established and how the formation of DNA loops can influence gene expression. We discuss the recent discoveries describing the 3D structure of the CTCF-DNA complex and the role of CTCF in establishing genome structure. Finally, we briefly explain how various genetic disorders might arise as a consequence of mutations in the CTCF target sequence or alteration of genomic imprinting.]]>
Wed, 31 Dec 1969 19:00:00 EST
Genome-wide screening and analysis of imprinted genes in rapeseed (Brassica napus L.) endosperm. Liu J, Li J, Liu HF, Fan SH, Singh S, Zhou XR, Hu ZY, Wang HZ, Hua W
DNA Res (Sep 2018)

Species-specific genomic imprinting is an epigenetic phenomenon leading to parent-of-origin-specific differential expression of maternally and paternally inherited alleles. To date, no studies of imprinting have been reported in rapeseed, a tetraploid species. Here, we analysed global patterns of allelic gene expression in developing rapeseed endosperms from reciprocal crosses between inbred lines YN171 and 93275. A total of 183 imprinted genes, consisting of 167 maternal expressed genes (MEGs) and 16 paternal expressed genes (PEGs), were identified from 14,394 genes found to harbour diagnostic SNPs between the parental lines. Some imprinted genes were validated in different endosperm stages and other parental combinations by RT-PCR analysis. A clear clustering of imprinted genes throughout the rapeseed genome was identified, which was different from most other plants. Methylation analysis of 104 out of the 183 imprinted genes showed that 11 genes (7 MEGs and 4 PEGs) harboured differentially methylated regions (DMRs). Unexpectedly, only 1 MEG out of these 11 genes had a DMR that exhibited high CG methylation rate in paternal allele and had big difference between parent alleles. These results extend our understanding of gene imprinting in plants and provide potential avenues for further research in imprinted genes.]]>
Wed, 31 Dec 1969 19:00:00 EST
Contemporary Trends Emerging in Epigenomics and Metabolism. El-Osta A
Antioxid Redox Signal (Oct 2018)

Diabetes is the disease of our time. It is a complex disorder. It is increasingly appreciated that genetic factors cannot fully explain susceptibility to diabetes and its complications. For almost a decade, the epigenetics field has grown tremendously becoming an alternative but integral component of how we interpret gene regulation. Some consider the field an epiphenomenon with an evidence base awaiting critical testing. The advent of experimental tools combined with the development of research methods has brought with the field technological advancements that allow scientists to assess ideas that have not yet been tested critically. If there was ever a time not to give up on epigenetics, then that time would be now. Under the seeming disorder of more than 3 billion base pairs, the human genome works successfully with order. It is a complex order. Instructed by a chemical code that is largely uncharted in metabolic disease, developmental studies have clearly shown that code exclusivity is key to unlocking the genetic blueprint. Central to this chemical code are specific modifications to DNA and RNA, histones and nonhistone proteins: these tiny chemical marks that have wide-ranging functions. Robustness is key, and these marks are written to be precisely read and accurately erased.]]>
Wed, 31 Dec 1969 19:00:00 EST
Long noncoding RNAs: regulation, function and cancer. Rafiee A, Riazi-Rad F, Havaskary M, Nuri F
Biotechnol Genet Eng Rev (Oct 2018)

Long noncoding RNAs (lncRNAs) are non-protein-coding RNA transcripts that exert a key role in many cellular processes and have potential toward addressing disease etiology. Here, we review existing noncoding RNA classes and then describe a variety of mechanisms and functions by which lncRNAs regulate gene expression such as chromatin remodeling, genomic imprinting, gene transcription and post-transcriptional processing. We also examine several lncRNAs that contribute significantly to pathogenesis, oncogenesis, tumor suppression and cell cycle arrest of diverse cancer types and also give a summary of the pathways that lncRNAs might be involved in.]]>
Wed, 31 Dec 1969 19:00:00 EST
Generation of Bimaternal and Bipaternal Mice from Hypomethylated Haploid ESCs with Imprinting Region Deletions. Li ZK, Wang LY, Wang LB, Feng GH, Yuan XW, Liu C, Xu K, Li YH, Wan HF, Zhang Y, Li YF, Li X, Li W, Zhou Q, Hu BY
Cell Stem Cell (Oct 2018)

Unisexual reproduction is widespread among lower vertebrates, but not in mammals. Deletion of the H19 imprinted region in immature oocytes produced bimaternal mice with defective growth; however, bipaternal reproduction has not been previously achieved in mammals. We found that cultured parthenogenetic and androgenetic haploid embryonic stem cells (haESCs) display DNA hypomethylation resembling that of primordial germ cells. Through MII oocyte injection or sperm coinjection with hypomethylated haploid ESCs carrying specific imprinted region deletions, we obtained live bimaternal and bipaternal mice. Deletion of 3 imprinted regions in parthenogenetic haploid ESCs restored normal growth of fertile bimaternal mice, whereas deletion of 7 imprinted regions in androgenetic haploid ESCs enabled production of live bipaternal mice that died shortly after birth. Phenotypic analyses of organ and body size of these mice support the genetic conflict theory of genomic imprinting. Taken together, our results highlight the factors necessary for crossing same-sex reproduction barriers in mammals.]]>
Wed, 31 Dec 1969 19:00:00 EST
Predictive biomarkers for type 2 of diabetes mellitus: Bridging the gap between systems research and personalized medicine. Kraniotou C, Karadima V, Bellos G, Tsangaris GT
J Proteomics (Sep 2018)

The global incidence of metabolic disorders like type 2 diabetes mellitus (DM2) has assumed epidemic proportions, leading to adverse health and socio-economic impacts. It is therefore of critical importance the early diagnosis of DM2 patients and the detection of those at increased risk of disease. In this respect, Precision Medicine (PM) is an emerging approach that includes practices, tests, decisions and treatments adapted to the characteristics of each patient. With regard to DM2, PM manages a wealth of "omics" data (genomic, metabolic, proteomic, environmental, clinical and paraclinical) to increase the number of clinically validated biomarkers in order to identify patients in early stage even before the prediabetic phase.]]>
Wed, 31 Dec 1969 19:00:00 EST
A comprehensive overview of genomic imprinting in breast and its deregulation in cancer. Goovaerts T, Steyaert S, Vandenbussche CA, Galle J, Thas O, Van Criekinge W, De Meyer T
Nat Commun (Oct 2018)

Genomic imprinting plays an important role in growth and development. Loss of imprinting (LOI) has been found in cancer, yet systematic studies are impeded by data-analytical challenges. We developed a methodology to detect monoallelically expressed loci without requiring genotyping data, and applied it on The Cancer Genome Atlas (TCGA, discovery) and Genotype-Tissue expression project (GTEx, validation) breast tissue RNA-seq data. Here, we report the identification of 30 putatively imprinted genes in breast. In breast cancer (TCGA), HM13 is featured by LOI and expression upregulation, which is linked to DNA demethylation. Other imprinted genes typically demonstrate lower expression in cancer, often associated with copy number variation and aberrant DNA methylation. Downregulation in cancer frequently leads to higher relative expression of the (imperfectly) silenced allele, yet this is not considered canonical LOI given the lack of (absolute) re-expression. In summary, our novel methodology highlights the massive deregulation of imprinting in breast cancer.]]>
Wed, 31 Dec 1969 19:00:00 EST
Super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers. Khan A, Mathelier A, Zhang X
Epigenetics (Oct 2018)

Super-enhancers and stretch enhancers represent classes of transcriptional enhancers that have been shown to control the expression of cell identity genes and carry disease- and trait-associated variants. Specifically, super-enhancers are clusters of enhancers defined based on the binding occupancy of master transcription factors, chromatin regulators, or chromatin marks, while stretch enhancers are large chromatin-defined regulatory regions of at least 3,000 base pairs. Several studies have characterized these regulatory regions in numerous cell types and tissues to decipher their functional importance. However, the differences and similarities between these regulatory regions have not been fully assessed. We integrated genomic, epigenomic, and transcriptomic data from ten human cell types to perform a comparative analysis of super and stretch enhancers with respect to their chromatin profiles, cell type-specificity, and ability to control gene expression. We found that stretch enhancers are more abundant, more distal to transcription start sites, cover twice as much the genome, and are significantly less conserved than super-enhancers. In contrast, super-enhancers are significantly more enriched for active chromatin marks and cohesin complex, and more transcriptionally active than stretch enhancers. Importantly, a vast majority of super-enhancers (85%) overlap with only a small subset of stretch enhancers (13%), which are enriched for cell type-specific biological functions, and control cell identity genes. These results suggest that super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers, and importantly, most of the stretch enhancers that are distinct from super-enhancers do not show an association with cell identity genes, are less active, and more likely to be poised enhancers.]]>
Wed, 31 Dec 1969 19:00:00 EST
Preliminary observations of mitochondrial dysfunction in Prader-Willi syndrome. Butler MG, Hossain WA, Tessman R, Krishnamurthy PC
Am J Med Genet A (Oct 2018)

Prader-Willi syndrome (PWS) is a complex multisystem disorder because of errors in genomic imprinting with severe hypotonia, decreased muscle mass, poor suckling, feeding problems and failure to thrive during infancy, growth and other hormone deficiency, childhood-onset hyperphagia, and subsequent obesity. Decreased energy expenditure in PWS is thought to contribute to reduced muscle mass and physical activity but may also relate to cellular metabolism and disturbances in mitochondrial function. We established fibroblast cell lines from six children and adults with PWS and six healthy controls for mitochondrial assays. We used Agilent Seahorse XF extracellular flux technology to determine real-time measurements of several metabolic parameters including cellular substrate utilization, Adenosine Triphosphate (ATP)-linked respiration, and mitochondrial capacity in living cells. Decreased mitochondrial function was observed in the PWS patients compared to the healthy controls with significant differences in basal respiration, maximal respiratory capacity, and ATP-linked respiration. These results suggest disturbed mitochondrial bioenergetics in PWS although the low number of studied subjects will require a larger subject population before a general consensus can be reached to identify if mitochondrial dysfunction is a contributing factor in PWS.]]>
Wed, 31 Dec 1969 19:00:00 EST
Beckwith-Wiedemann syndrome: clinical and etiopathogenic aspects of a model genomic imprinting entity. Cammarata-Scalisi F, Avendaño A, Stock F, Callea M, Sparago A, Riccio A
Arch Argent Pediatr (Oct 2018)

The Beckwith-Wiedemann syndrome is the most common genetic entity in overgrowth, with an approximate incidence of 1 in 10 00013 700births. Its broad clinical spectrum includes pre- and postnatal macrosomia, macroglossia, pinna abnormalities, abdominal wall defects, visceromegaly, and hyperinsulinemic hypoglycemia. This syndrome predisposes to childhood cancer and is caused by diverse genetic and/or epigenetic disorders that usually affect the regulation of genes imprinted on chromosome 11p15.5. The knowledge of (epi) genotype-phenotype correlations has prompted recommendations to propose different health care strategies, including tumor surveillance protocols based on molecular classification, aimed at standardizing clinical practice. The objective of this article is to describe the current status of the Beckwith-Wiedemann syndrome, a model of genomic imprinting.]]>
Wed, 31 Dec 1969 19:00:00 EST
Functional conservation of sequence determinants at rapidly evolving regulatory regions across mammals. Huh I, Mendizabal I, Park T, Yi SV
PLoS Comput Biol (Oct 2018)

Recent advances in epigenomics have made it possible to map genome-wide regulatory regions using empirical methods. Subsequent comparative epigenomic studies have revealed that regulatory regions diverge rapidly between genome of different species, and that the divergence is more pronounced in enhancers than in promoters. To understand genomic changes underlying these patterns, we investigated if we can identify specific sequence fragments that are over-enriched in regulatory regions, thus potentially contributing to regulatory functions of such regions. Here we report numerous sequence fragments that are statistically over-enriched in enhancers and promoters of different mammals (which we refer to as 'sequence determinants'). Interestingly, the degree of statistical enrichment, which presumably is associated with the degree of regulatory impacts of the specific sequence determinant, was significantly higher for promoter sequence determinants than enhancer sequence determinants. We further used a machine learning method to construct prediction models using sequence determinants. Remarkably, prediction models constructed from one species could be used to predict regulatory regions of other species with high accuracy. This observation indicates that even though the precise locations of regulatory regions diverge rapidly during evolution, the functional potential of sequence determinants underlying regulatory sequences may be conserved between species.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetics and Epigenomics: Implications for Diabetes and Obesity. Rosen ED, Kaestner KH, Natarajan R, Patti ME, Sallari R, Sander M, Susztak K
Diabetes (10 2018)

The American Diabetes Association convened a research symposium, "Epigenetics and Epigenomics: Implications for Diabetes and Obesity" on 17-19 November 2017. International experts in genetics, epigenetics, computational biology, and physiology discussed the current state of understanding of the relationships between genetics, epigenetics, and environment in diabetes and examined existing evidence for the role of epigenetic factors in regulating metabolism and the risk of diabetes and its complications. The authors summarize the presentations, which highlight how the complex interactions between genes and environment may in part be mediated through epigenetic changes and how information about nutritional and other environmental stimuli can be transmitted to the next generation. In addition, the authors present expert consensus on knowledge gaps and research recommendations for the field.]]>
Wed, 31 Dec 1969 19:00:00 EST
A Loss of Epigenetic Control Can Promote Cell Death through Reversing the Balance of Pathways in a Signaling Network. Vanaja KG, Timp W, Feinberg AP, Levchenko A
Mol Cell (Oct 2018)

Epigenetic control of regulatory networks is only partially understood. Expression of Insulin-like growth factor-II (IGF2) is controlled by genomic imprinting, mediated by silencing of the maternal allele. Loss of imprinting of IGF2 (LOI) is linked to intestinal and colorectal cancers, causally in murine models and epidemiologically in humans. However, the molecular underpinnings of the LOI phenotype are not clear. Surprisingly, in LOI cells, we find a reversal of the relative activities of two canonical signaling pathways triggered by IGF2, causing further rebalancing between pro- and anti-apoptotic signaling. A predictive mathematical model shows that this network rebalancing quantitatively accounts for the effect of receptor tyrosine kinase inhibition in both WT and LOI cells. This mechanism also quantitatively explains both the stable LOI phenotype and the therapeutic window for selective killing of LOI cells, and thus prevention of epigenetically controlled cancers. These findings suggest a framework for understanding epigenetically modified cell signaling.]]>
Wed, 31 Dec 1969 19:00:00 EST
Maintenance of grafting-induced epigenetic variations in the asexual progeny of Brassica oleracea and B. juncea chimera. Yu N, Cao L, Yuan L, Zhi X, Chen Y, Gan S, Chen L
Plant J (Oct 2018)

Grafting-induced variations have been observed in many plant species, but the heritability of variation in progeny is not well understood. In our study, adventitious shoots from the C cell lineage of shoot apical meristem (SAM) grafting chimera TCC (where the origin of the outmost, middle and innermost cell layers, respectively, of SAM is designated by 'T' for tuber mustard and 'C' for red cabbage) were induced and identified as r-CCC (r = regenerated). To investigate the maintenance of grafting variations during cell propagation and regeneration, different generations of asexual progeny (r-CCCn, n = generation) were established through successive regeneration of axillary shoots from r-CCC. The fourth generation of r-CCC (r-CCC4) was selected to perform whole genome bisulfite sequencing for comparative analysis of hetero-grafting-induced global methylation changes relative to r-s-CCC4 (s = self-grafting). Increased CHH methylation levels and proportions were observed in r-CCC4, with substantial changes occurring in the repeat elements. Small RNA sequencing revealed 1135 specific small interfering RNA (siRNA) tags that were typically expressed in r-CCC, r-CCC2 and r-CCC4. Notably, 65% of these specific siRNAs were associated with repeat elements, termed RE siRNAs. Subsequent analysis revealed that the CHH methylation of RE siRNA-overlapping regions was mainly hypermethylation in r-CCC4, indicating that they were responsible for directing and maintaining grafting-induced CHH methylation. Moreover, the expression of 13 differentially methylated genes (DMGs) correlated with the phenotypic variation, showing differential expression levels between r-CCC4 and r-s-CCC4. These DMGs were predominantly CG hypermethylated, their methylation modifications corresponded to the transcription of relative methyltransferase.]]>
Wed, 31 Dec 1969 19:00:00 EST
Intersexual conflict over seed size is stronger in more outcrossed populations of a mixed-mating plant. Raunsgard A, Opedal Ã˜H, Ekrem RK, Wright J, Bolstad GH, Armbruster WS, Pélabon C
Proc Natl Acad Sci U S A (Oct 2018)

In polyandrous species, fathers benefit from attracting greater maternal investment toward their offspring at the expense of the offspring of other males, while mothers should usually allocate resources equally among offspring. This conflict can lead to an evolutionary arms race between the sexes, manifested through antagonistic genes whose expression in offspring depends upon the parent of origin. The arms race may involve an increase in the strength of maternally versus paternally derived alleles engaged in a "tug of war" over maternal provisioning or repeated "recognition-avoidance" coevolution where growth-enhancing paternally derived alleles evolve to escape recognition by maternal genes targeted to suppress their effect. Here, we develop predictions to distinguish between these two mechanisms when considering crosses among populations that have reached different equilibria in this intersexual arms race. We test these predictions using crosses within and among populations of (Euphorbiaceae) that presumably have experienced different intensities of intersexual conflict, as inferred from their historical differences in mating system. In crosses where the paternal population was more outcrossed than the maternal population, hybrid seeds were larger than those normally produced in the maternal population, whereas when the maternal population was more outcrossed, hybrid seeds were smaller than normal. These results confirm the importance of mating systems in determining the intensity of intersexual conflict over maternal investment and provide strong support for a tug-of-war mechanism operating in this conflict. They also yield clear predictions for the fitness consequences of gene flow among populations with different mating histories.]]>
Wed, 31 Dec 1969 19:00:00 EST
Identification of a novel antisense noncoding RNA, ALID, transcribed from the putative imprinting control region of marsupial IGF2R. Suzuki S, Shaw G, Renfree MB
Epigenetics Chromatin (09 2018)

Genomic imprinting leads to maternal expression of IGF2R in both mouse and opossum. In mouse, the antisense long noncoding (lnc) RNA Airn, which is paternally expressed from the differentially methylated region (DMR) in the second intron of Igf2r, is required to silence the paternal Igf2r. In opossum, however, intriguingly, the DMR was reported to be in a different downstream intron (intron 11) and there was no antisense lncRNA detected in previous analyses. Therefore, clarifying the imprinting mechanism of marsupial IGF2R is of great relevance for understanding the origin and evolution of genomic imprinting in the IGF2R locus. Thus, the antisense lncRNA associated with the marsupial DMR can be considered as the 'missing link'. In this study, we identified a novel antisense lncRNA, ALID, after detailed analysis of the IGF2R locus in an Australian marsupial, the tammar wallaby, Macropus eugenii, and compared it to that of the grey short-tailed opossum, Monodelphis domestica.]]>
Wed, 31 Dec 1969 19:00:00 EST
Biochemical and Pharmacological Applications of Essential Oils in Human Health Especially in Cancer Prevention. Miahra SK, Ishfaq PM, Tripathi S, Shukla A, Beraiya S
Anticancer Agents Med Chem (Oct 2018)

Background - At present, 'pharmaco-epigenomics' constitutes the hope in cancer treatment owing to epigenetic deregulation- a reversible process and playing a role in malignancy.]]>
Wed, 31 Dec 1969 19:00:00 EST
DNA demethylase ROS1 negatively regulates the imprinting of and seed dormancy in . Zhu H, Xie W, Xu D, Miki D, Tang K, Huang CF, Zhu JK
Proc Natl Acad Sci U S A (Sep 2018)

Genomic imprinting is a form of epigenetic regulation resulting in differential gene expression that reflects the parent of origin. In plants, imprinted gene expression predominantly occurs in the seed endosperm. Maternal-specific DNA demethylation by the DNA demethylase DME frequently underlies genomic imprinting in endosperm. Whether other more ubiquitously expressed DNA demethylases regulate imprinting is unknown. Here, we found that the DNA demethylase ROS1 regulates the imprinting of is expressed from the maternal allele in endosperm and displays preferential methylation and suppression of the paternal allele. We found that ROS1 negatively regulates imprinting by demethylating the paternal allele, preventing its hypermethylation and complete silencing. Furthermore, we found that negatively affects seed dormancy and response to the phytohormone abscisic acid and that ROS1 controls these processes by regulating Our results reveal roles for ROS1 in mitigating imprinted gene expression and regulating seed dormancy.]]>
Wed, 31 Dec 1969 19:00:00 EST