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Expansins, cell wall proteins, play a significant role in plant stress resistance. Our previous study confirmed the expression of the expansin gene SmEXPA13 from Salix matsudana Koidz. enhanced salt tolerance of plants. This report presented an assay that the expression of SmEXPA13 was higher in the salt-resistant willow variety 9901 than in the salt-sensitive variety Yanjiang. In order to understand the possible reasons, a study of the regulation process was conducted. Despite being cloned from both varieties, SmEXPA13 and its promotor showed no significant differences in the structure and sequence. A transcription factor (TF), SmMYB1R1-L, identified through screening the yeast library of willow cDNA, was found to regulate SmEXPA13. Yeast one-hybrid (Y1H) assay confirmed that SmMYB1R1-L could bind to the MYB element at the -520 bp site on the SmEXPA13 promotor. A dual-luciferase reporter assay also demonstrated that SmMYB1R1-L could greatly activate SmEXPA13 expression. The willow calli with over-expression of SmMYB1R1-L exhibited better physiological performance than the wild type under salt stress. Further testing the expression of SmMYB1R1-L displayed it significantly higher in 9901 willow than that in Yanjiang under salt stress. In conclusion, the high accumulation of SmMYB1R1-L in 9901 willow under salt stress led to the high expression of SmEXPA13, resulting in variations in salt stress resistance among willow varieties. The SmMYB1R1-L/SmEXPA13 cascade module in willow offers a new perspective on plant resistance mechanisms., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest or competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Knowledge of the transcription factor binding landscape (TFBL) is necessary to analyze gene regulatory networks for important agronomic traits. However, a low-cost and high-throughput in vivo chromatin profiling method is still lacking in plants. Here, we developed a transient and simplified cleavage under targets and tagmentation (tsCUT&Tag) that combines transient expression of transcription factor proteins in protoplasts with a simplified CUT&Tag without nucleus extraction. Our tsCUT&Tag method provided higher data quality and signal resolution with lower sequencing depth compared with traditional ChIP-seq. Furthermore, we developed a strategy combining tsCUT&Tag with machine learning, which has great potential for profiling the TFBL across plant development., (© 2022 Institute of Botany, Chinese Academy of Sciences.)

Translational regulation plays a critical role during the oocyte-to-embryo transition (OET) and zygotic genome activation (ZGA). Here, we integrated ultra-low-input ribosome profiling (Ribo-lite) with messenger RNA sequencing to co-profile the translatome and transcriptome in human oocytes and early embryos. Comparison with mouse counterparts identified widespread differentially translated gene functioning in epigenetic reprogramming, transposon defense, and small RNA biogenesis, in part driven by species-specific regulatory elements in 3' untranslated regions. Moreover, PRD-like homeobox transcription factors, including TPRXL , TPRX1 , and TPRX2 , are highly translated around ZGA. TPRX1/2/L knockdown leads to defective ZGA and preimplantation development. Ectopically expressed TPRXs bind and activate key ZGA genes in human embryonic stem cells. These data reveal the conservation and divergence of translation landscapes during OET and identify critical regulators of human ZGA.

Background: ARID1A is an essential subunit of SWI/SNF chromatin remodeling complexes. ARID1A gene mutations and loss of ARID1A expression have been observed in a variety of cancers, and to be correlated with invasion, immune escape and synthetic lethality. As yet, however, the biological effect of ARID1A expression and its role in the prognosis of lung adenocarcinoma (LUAD) patients have remained unclear. In this study we aimed to further elucidate the role of ARID1A expression in LUAD in vitro and in vivo and to assess its effect on the clinical prognosis of LUAD patients., Methods: ARID1A expression was detected by IHC in tissue samples from LUAD patients. After regular culturing of LUAD cell lines and constructing stable ARID1A knockdown lines, wound healing and Transwell assays were used to assess the role of ARID1A in cell migration and invasion. The effect of ARID1A knockdown on metastasis was verified in vivo. Western blotting was used to examine the expression of target proteins. Univariate and multivariate analyses were performed to assess survival and to provide variables for nomogram construction. In addition, we used the "rms" package to construct a prognostic nomogram based on a Cox regression model., Results: We found that ARID1A expression serves as an effective prognostic marker for LUAD patients. Loss of ARID1A expression correlated with a poor prognosis, as verified with a nomogram based on a Cox regression model. In addition, we found that ARID1A knockdown promoted LUAD cell proliferation, migration and invasion in vitro and enhanced LUAD metastasis in vivo by activating the Akt signaling pathway., Conclusions: Our data indicate that loss of ARID1A expression promotes LUAD metastasis and predicts a poor prognosis in LUAD patients., (© 2021. Springer Nature Switzerland AG.)

Ovarian cancer (OC) is the deadliest gynecological malignancy. The pathogenesis of molecular in epithelial ovarian cancer (EOC), main histological type of OC, has not been completely defined. Enhancer of rudimentary homolog (ERH) had been reported to participate in transcriptional regulation, mRNA splicing, DNA repair and DNA synthesis by binding a variety of proteins. In this study, immunohistochemical staining revealed that the protein expression of ERH was associated with histological type, lymph node metastasis and pathological grade in EOC patients. To verify the association of ERH with the prognosis of OC, a GSE microarray dataset was downloaded from the Gene Expression Omnibus (GEO) database. Survival analysis suggested that ERH may be associated with poor prognosis of OC. In addition, shRNA was used to knockdown the protein and mRNA expression levels of ERH in the OC cell line SKOV3. Inhibition of ERH expression slowed proliferation, promoted apoptosis and inhibited metastasis and invasion by regulating epithelial-mesenchymal transition (EMT) in SKOV3 cells. These results indicate that ERH protein promotes the development of OC and provides an experimental basis for ERH as the potential target for ovarian cancer treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest and nothing to disclose., (Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Maize exhibits marked growth and yield response to supplemental nitrogen (N). Here, we report the functional characterization of a maize NIN-like protein ZmNLP5 as a central hub in a molecular network associated with N metabolism. Predominantly expressed and accumulated in roots and vascular tissues, ZmNLP5 was shown to rapidly respond to nitrate treatment. Under limited N supply, compared with that of wild-type (WT) seedlings, the zmnlp5 mutant seedlings accumulated less nitrate and nitrite in the root tissues and ammonium in the shoot tissues. The zmnlp5 mutant plants accumulated less nitrogen than the WT plants in the ear leaves and seed kernels. Furthermore, the mutants carrying the transgenic ZmNLP5 cDNA fragment significantly increased the nitrate content in the root tissues compared with that of the zmnlp5 mutants. In the zmnlp5 mutant plants, loss of the ZmNLP5 function led to changes in expression for a significant number of genes involved in N signalling and metabolism. We further show that ZmNLP5 directly regulates the expression of nitrite reductase 1.1 (ZmNIR1.1) by binding to the nitrate-responsive cis-element at the 5' UTR of the gene. Interestingly, a natural loss-of-function allele of ZmNLP5 in Mo17 conferred less N accumulation in the ear leaves and seed kernels resembling that of the zmnlp5 mutant plants. Our findings show that ZmNLP5 is involved in mediating the plant response to N in maize., (© 2019 The Authors. The Plant Journal published by Society for Experimental Biology and John Wiley & Sons Ltd.)

Objective: To investigate whether LHX1 gene mutations exist in Han Chinese patients with müllerian duct abnormalities (MDAs)., Design: Mutation screening., Setting: University hospital., Patient(s): Ninety-six MDA patients and 105 control subjects from a Han Chinese population. The parents of the patients carrying the genetic variation were also screened., Intervention(s): Gene sequencing., Main Outcome Measure(s): Karyotype, LHX1 gene sequencing., Result(s): We found no significant mutation in coding regions of LHX1. However, there is a new rare polymorphism of LHX1 gene, c.1070-1081del, found in 1 out of 77 incomplete müllerian fusion patients and 1 out of 105 control individuals in the Han Chinese population (thus affecting ∼1% of Han Chinese)., Conclusion(s): No causative perturbation was identified in the LHX1 gene. Mutations in the coding regions of LHX1 may not be a common genetic etiologic factor involved in Han Chinese MDA patients., (Copyright © 2012 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.)

NOBOX (newborn ovary homeobox gene) is an oocyte-specific homeobox gene that plays a critical role in early folliculogenesis and represents a candidate gene for nonsyndromic ovarian failure. We investigated whether mutations in the NOBOX gene cause premature ovarian failure (POF). We sequenced the NOBOX gene in 96 white women with POF and discovered seven known single-nucleotide polymorphisms and four novel variations, two of which, p.Arg355His and p.Arg360Gln, cause missense mutations in the homeobox domain. Electrophoretic mobility shift assay (EMSA) confirmed that the missense mutation, p.Arg355His, disrupted NOBOX homeodomain binding to NOBOX DNA-binding element (NBE) and had a dominant negative effect on the binding of wild-type NOBOX to DNA. Our findings demonstrate that NOBOX mutations can cause POF.

The B3 superfamily, which belongs to the plant-specific transcription factors, is widely involved in multiple biological processes. In apricot (Prunus armeniaca), the classification, structure, and function of the B3 superfamily are not yet clear. In this study, a total of 75 B3 genes were identified from the apricot genome. The apricot B3 superfamily can be divided into five subfamilies, i.e., REM, ARF, ABI3, RAV, and HSI, and genes in the same subfamily have similar structures. The distribution of B3 genes on chromosomes presents a clustering phenomenon. Tandem duplication is the main mode of apricot B3 family expansion, and gene duplication mainly occurs in the REM and ARF subfamilies. Many B3 genes originated from a common ancestor of Arabidopsis and apricot before lineage divergence, and ancestor genes expanded fewer times in apricot than in Arabidopsis. Gene ontology analysis showed that apricot B3 genes were closely related to vernalization, flower development, and shoot system development. PaABI3-1 and PaABI3-2 might play a positive regulation role in the transcription of PaOleosin, which encodes a lipid body protein. This study lays a foundation for the further study of the B3 superfamily function in apricot, especially the specific functions of the ABI3 subfamily in apricot kernel oil storage. [ABSTRACT FROM AUTHOR]

Insulin/IGF-1 Signaling (IIS) is known to constrain longevity by inhibiting the transcription factor FOXO. How phosphorylation mediated by IIS kinases regulates lifespan beyond FOXO remains unclear. Here, we profile IIS-dependent phosphorylation changes in a large-scale quantitative phosphoproteomic analysis of wild-type and three IIS mutant Caenorhabditis elegans strains. We quantify more than 15,000 phosphosites and find that 476 of these are differentially phosphorylated in the long-lived daf-2/insulin receptor mutant. We develop a machine learning-based method to prioritize 25 potential lifespan-related phosphosites. We perform validations to show that AKT-1 pT492 inhibits DAF-16/FOXO and compensates the loss of daf-2 function, that EIF-2α pS49 potently inhibits protein synthesis and daf-2 longevity, and that reduced phosphorylation of multiple germline proteins apparently transmits reduced DAF-2 signaling to the soma. In addition, an analysis of kinases with enriched substrates detects that casein kinase 2 (CK2) subunits negatively regulate lifespan. Our study reveals detailed functional insights into longevity. How phosphorylation mediated by Insulin/IGF-1 Signaling kinases regulates lifespan remains unclear. Here the authors perform a large-scale quantitative phosphoproteomic analysis of wildtype and IIS mutant C. elegans strains to reveal detailed functional insights into longevity. [ABSTRACT FROM AUTHOR]

Background: The fluctuation of nitrogen (N) contents profoundly affects the root growth and architecture in maize by altering the expression of thousands of genes. The differentially expressed genes (DEGs) in response to N have been extensively reported. However, information about the effects of N variation on the alternative splicing in genes is limited. Results: To reveal the effects of N on the transcriptome comprehensively, we studied the N-starved roots of B73 in response to nitrate treatment, using a combination of short-read sequencing (RNA-seq) and long-read sequencing (PacBio-sequencing) techniques. Samples were collected before and 30 min after nitrate supply. RNA-seq analysis revealed that the DEGs in response to N treatment were mainly associated with N metabolism and signal transduction. In addition, we developed a workflow that utilizes the RNA-seq data to improve the quality of long reads, increasing the number of high-quality long reads to about 2.5 times. Using this workflow, we identified thousands of novel isoforms; most of them encoded the known functional domains and were supported by the RNA-seq data. Moreover, we found more than 1000 genes that experienced AS events specifically in the N-treated samples, most of them were not differentially expressed after nitrate supply-these genes mainly related to immunity, molecular modification, and transportation. Notably, we found a transcription factor ZmNLP6, a homolog of AtNLP7-a well-known regulator for N-response and root growth-generates several isoforms varied in capacities of activating downstream targets specifically after nitrate supply. We found that one of its isoforms has an increased ability to activate downstream genes. Overlaying DEGs and DAP-seq results revealed that many putative targets of ZmNLP6 are involved in regulating N metabolism, suggesting the involvement of ZmNLP6 in the N-response. Conclusions: Our study shows that many genes, including the transcription factor ZmNLP6, are involved in modulating early N-responses in maize through the mechanism of AS rather than altering the transcriptional abundance. Thus, AS plays an important role in maize to adapt N fluctuation. [ABSTRACT FROM AUTHOR]

Oxidative stress has been associated with the etipathogenesis of Diabetic retinopathy (DR). Studies have shown that DJ-1 plays an important role in regulating the reactive oxygen species (ROS) production and resistance to oxidative stress-induced apoptosis. This study aimed to investigate whether DJ-1 upregulates oxidative stress and prevents damage to retinal capillary pericytes by increasing antioxidant capacity through the Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Nrf2 is a redox-sensitive transcription factor that encode antioxidant enzymes and phase II metabolic enzymes, activation of Nrf2 functions is one of the critical defensive mechanisms against oxidative stress in many tissues. Our results showed after DJ-1 overexpression, apoptosis of rat retinal pericytes (RRPs) decreased, the ratio of B-cell lymphoma-2 (Bcl-2) to BCL2-Associated X Protein (BAX) increased, the production of ROS decreased, and the protein expression and activity of manganese superoxide dismutase (MnSOD, also called SOD2) and catalase (CAT) increased. DJ-1 overexpression activated Nrf2 expression, however, after Nrf2 silencing, apoptosis of RRPs increased, the ratio of Bcl-2 to BAX decreased, the production of ROS increased, the protein expression of MnSOD and CAT decreased, and the expression of heme oxygenase-1 (HO-1), NADP(H) quinone oxidoreductase (NQO1), glutamate-cysteine ligase catalytic subunit (GCLC) and modifier subunit (GCLM) decreased. These data suggest that enhancement of the Nrf2 pathway is a potential protective strategy for the treatment of DR. Therefore, DJ-1 may prevent high glucose-induced oxidative stress and RRPs apoptosis through the Nrf2 signaling pathway, thereby preventing the early onset and progression of DR. [ABSTRACT FROM AUTHOR]

Rapamycin (Rap) and its derivatives, called rapalogs, are being explored in clinical trials targeting cancer and neurodegeneration. The underlying mechanisms of Rap actions, however, are not well understood. Mechanistic target of rapamycin (mTOR), a lysosome-localized protein kinase that acts as a critical regulator of cellular growth, is believed to mediate most Rap actions. Here, we identified mucolipin 1 (transient receptor potential channel mucolipin 1 [TRPML1], also known as MCOLN1), the principle Ca2+ release channel in the lysosome, as another direct target of Rap. Patch-clamping of isolated lysosomal membranes showed that micromolar concentrations of Rap and some rapalogs activated lysosomal TRPML1 directly and specifically. Pharmacological inhibition or genetic inactivation of mTOR failed to mimic the Rap effect. In vitro binding assays revealed that Rap bound directly to purified TRPML1 proteins with a micromolar affinity. In both healthy and disease human fibroblasts, Rap and rapalogs induced autophagic flux via nuclear translocation of transcription factor EB (TFEB). However, such effects were abolished in TRPML1-deficient cells or by TRPML1 inhibitors. Hence, Rap and rapalogs promote autophagy via a TRPML1-dependent mechanism. Given the demonstrated roles of TRPML1 and TFEB in cellular clearance, we propose that lysosomal TRPML1 may contribute a significant portion to the in vivo neuroprotective and anti-aging effects of Rap via an augmentation of autophagy and lysosomal biogenesis. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) is a heterogeneous disorder characterized by chronic ovulatory dysfunction, hyperandrogenism, and polycystic ovaries. Wilms' tumor 1 (WT1) encoding a transcription factor involved in the differentiation of granulosa cells (GCs) regulates androgen receptor in the development of male genitalia. However, the expression pattern and possible role of WT1 in ovaries of PCOS patients are still unknown.Methods: GCs from 95 PCOS patients (PCOS group) and 62 healthy controls (control group) were isolated. The expression of WT1 in GCs was quantified using the reverse transcription-polymerase chain reaction. The correlation between WT1 expression and clinical characteristics was evaluated in PCOS patients.Results: WT1 expression was increased in PCOS patients compared with the normal controls. The expression of WT1 was moderately correlated with testosterone (r = 0.334, p = 0.001) and luteinizing hormone (r = 0.357, p = 0.001) levels and the antral follicle counts (r = 0.337, p = 0.001).Conclusions: Our study provided novel insights into the relationship between hyperandrogenism and polycystic ovaries of PCOS and WT1. [ABSTRACT FROM AUTHOR]

Atonal homolog 1 (Atoh1) is a basic helix-loop-helix transcription factor that is essential for inner ear hair cell differentiation. Previous studies have reported that Atoh1 gene transfer induces the production of ectopic hair cell-like cells (EHCLCs). In the present study, the effect of different Atoh1 expression levels and the duration of EHCLC formation on the lesser epithelial ridge (LER) of cochleae was examined using a human adenovirus serotype 5 (Ad5) vector encoding atoh1 and the reporter gene EGFP. Different Ad5-EGFP-atoh1/Ad5-EGFP virus titers were added to cultured cochlear explants and EHCLCs were detected in the LER at various time points. The results demonstrated that GFP alone did not induce EHCLCs. By contrast, Atoh1 expression induced EHCLCs as early as 2.5-5 days following EGFP-atoh1 infection in the LER and depending upon the viral titer, the number of EHCLCs increased with time. Higher Ad5-EGFP-atoh1 titers induced enhanced Atoh1 expression, resulting in an increase in EHCLCs. Lower Ad5-EGFP-atoh1 titers required more time for EHCLC formation and very low titers of Ad5-EGFP-atoh1 induced only weak Atoh1 expression and did not trigger EHCLC formation. In conclusion, the present study utilized an appropriate Ad5-EGFP-atoh1 titer range to induce Atoh1 expression and the subsequent production of EHCLCs. The results revealed that the Atoh1 expression level defined the fate of LER cells as either EHCLCs or nonsensory epithelial cells. This evidence may provide an important guideline for future studies into gene therapy strategies for the treatment of deafness. [ABSTRACT FROM AUTHOR]

Plants have evolved complex mechanisms to respond to the fluctuation of available nitrogen (N) in soil, but the genetic mechanisms underlying the N response in crops are not well-documented. In this study, we generated a time series of NO3−-mediated transcriptional profiles in roots of maize and sorghum, respectively. Using weighted gene co-expression network analysis, we identified modules of co-expressed genes that related to NO3− treatments. A cross-species comparison revealed 22 conserved modules, of which four were related to hormone signaling, suggesting that hormones participate in the early nitrate response. Three other modules are composed of genes that are mainly upregulated by NO3− and involved in nitrogen and carbohydrate metabolism, including NRT, NIR, NIA, FNR, and G6PD2. Two G2-like transcription factors (ZmNIGT1 and SbNIGT1), induced by NO3− stimulation, were identified as hub transcription factors (TFs) in the modules. Transient assays demonstrated that ZmNIGT1 and SbNIGT1 are transcriptional repressors. We identified the target genes of ZmNIGT1 by DNA affinity-purification sequencing (DAP-Seq) and found that they were significantly enriched in catalytic activity, including carbon, nitrogen, and other nutrient metabolism. A set of ZmNIGT1 targets encode transcription factors (ERF, ARF, and AGL) that are involved in hormone signaling and root development. We propose that ZmNIGT1 and SbNIGT1 are negative regulators of nitrate responses that play an important role in optimizing nutrition metabolism and root morphogenesis. Together with conserved N responsive modules, our study indicated that, to encounter N variation in soil, maize and sorghum have evolved an NO3−-regulatory network containing a set of conserved modules and transcription factors. [ABSTRACT FROM AUTHOR]

The roles and regulatory mechanisms of transcriptome changes during aging are unclear. It has been proposed that the transcriptome suffers decay during aging owing to age‐associated down‐regulation of transcription factors. In this study, we characterized the role of a transcription factor DAF‐16, which is a highly conserved lifespan regulator, in the normal aging process of Caenorhabditis elegans. We found that DAF‐16 translocates into the nucleus in aged wild‐type worms and activates the expression of hundreds of genes in response to age‐associated cellular stress. Most of the age‐dependent DAF‐16 targets are different from the canonical DAF‐16 targets downstream of insulin signaling. This and other evidence suggest that activation of DAF‐16 during aging is distinct from activation of DAF‐16 due to reduced signaling from DAF‐2. Further analysis showed that it is due in part to a loss of proteostasis during aging. We also found that without daf‐16, dramatic gene expression changes occur as early as on adult day 2, indicating that DAF‐16 acts to stabilize the transcriptome during normal aging. Our results thus reveal that normal aging is not simply a process in which the gene expression program descends into chaos due to loss of regulatory activities; rather, there is active transcriptional regulation during aging. [ABSTRACT FROM AUTHOR]

Huaren apricot and almond are two tree species with nuts as the main economically important products. Crossbreeding these two species might be a good approach for combining the traits of large seed kernel of almond with the wide adaptability of Huaren apricot. However, the molecular mechanism of hybridization incompatibility between Huaren apricot and almond has remained unclear until date. In the present study the transcriptomes of developing fruits after interspecific hybridization between Huaren apricot and almond and after intraspecific hybridization of Huaren apricot were compared to elucidate the possible molecular mechanisms of fruit development at the gene expression level. Approximately 562,535,240 clean reads were assembled, and 25,692 unigenes were identified. Totally, 270 differentially expressed genes (DEGs) were identified, of which 221 were up-regulated and 49 were down-regulated in almond as compared with Huaren apricot. Functional annotation analysis indicated that the expression of cinnamyl alcohol dehydrogenase and EREBP were significantly up-regulated, whereas GA2ox and MADS were down-regulated in the intraspecific hybridization (PN) as compared with the interspecific hybridization (MN). Moreover, these genes might play an important role in fruit development. This study provides novel insights into the molecular mechanisms of fruit development in interspecific and intraspecific hybrids. [ABSTRACT FROM AUTHOR]

Fluctuations in nitrogen (N) availability influence protein and starch levels in maize (Zea mays) seeds, yet the underlying mechanism is not well understood. Here, we report that N limitation impacted the expression of many key genes in N and carbon (C) metabolism in the developing endosperm of maize. Notably, the promoter regions of those genes were enriched for P-box sequences, the binding motif of the transcription factor prolamin-box binding factor 1 (PBF1). Loss of PBF1 altered accumulation of starch and proteins in endosperm. Under different N conditions, PBF1 protein levels remained stable but PBF1 bound different sets of target genes, especially genes related to the biosynthesis and accumulation of N and C storage products. Upon N-starvation, the absence of PBF1 from the promoters of some zein genes coincided with their reduced expression, suggesting that PBF1 promotes zein accumulation in the endosperm. In addition, PBF1 repressed the expression of sugary1 (Su1) and starch branching enzyme 2b (Sbe2b) under normal N supply, suggesting that, under N-deficiency, PBF1 redirects the flow of C skeletons for zein toward the formation of C compounds. Overall, our study demonstrates that PBF1 modulates C and N metabolism during endosperm development in an N-dependent manner. Prolamin-box-binding factor 1 is a key transcription factor that balances protein and carbohydrate storage in maize endosperm by binding to the promoters of target genes in a nitrogen-dependent manner. [ABSTRACT FROM AUTHOR]

Gene expression is regulated at many different levels during the life cycle of all plant species. Recent investigations have taken advantage of next-generation sequencing to study the relevance of DNA methylation and sRNAs in controlling tissue-specific gene expression in maize at the genome-wide level. Here, we profiled H3K27ac in maize, which has one of the largest sequenced plant genomes due to the amplification of retrotransposons. Because transcribed genes represent only a small proportion of its genome, gene-specific epigenetic modifications are concentrated in a relatively small percentage of the genome. Indeed, H3K27ac marks are mostly in gene-rich, in contrast to gene-poor regions. A large proportion of those marks are located in transcribed regions of genes, including 111 out of 458 known genetic loci. Moreover, increased transcription correlates with the presence of H3K27ac modification in gene bodies. Using maize as an example, we suggest that H3K27ac marks actively transcribed genes in plants. [ABSTRACT FROM AUTHOR]