'; ?> 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, 18 Sep 2020 16:39:19 EDT Fri, 18 Sep 2020 16:39:19 EDT jirtle@radonc.duke.edu james001@jirtle.com Insights into glucocorticoid responses derived from omics studies. Kan M, Himes BE
Pharmacol Ther (Sep 2020)

Glucocorticoid drugs are commonly used in the treatment of several conditions, including autoimmune diseases, asthma and cancer. Despite their widespread use and knowledge of biological pathways via which they act, much remains to be learned about the cell type-specific mechanisms of glucocorticoid action and the reasons why patients respond differently to them. In recent years, human and in vitro studies have addressed these questions with genomics, transcriptomics and other omics approaches. Here, we summarize key insights derived from omics studies of glucocorticoid response, and we identify existing knowledge gaps related to mechanisms of glucocorticoid action that future studies can address.]]>
Wed, 31 Dec 1969 19:00:00 EST
Setd1a Insufficiency in Mice Attenuates Excitatory Synaptic Function and Recapitulates Schizophrenia-Related Behavioral Abnormalities. Nagahama K, Sakoori K, Watanabe T, Kishi Y, Kawaji K, Koebis M, Nakao K, Gotoh Y, Aiba A, Uesaka N, Kano M
Cell Rep (Sep 2020)

SETD1A encodes a histone methyltransferase whose de novo mutations are identified in schizophrenia (SCZ) patients and confer a large increase in disease risk. Here, we generate Setd1a mutant mice carrying the frameshift mutation that closely mimics a loss-of-function variant of SCZ. Our Setd1a (+/-) mice display various behavioral abnormalities relevant to features of SCZ, impaired excitatory synaptic transmission in layer 2/3 (L2/3) pyramidal neurons of the medial prefrontal cortex (mPFC), and altered expression of diverse genes related to neurodevelopmental disorders and synaptic functions in the mPFC. RNAi-mediated Setd1a knockdown (KD) specifically in L2/3 pyramidal neurons of the mPFC only recapitulates impaired sociality among multiple behavioral abnormalities of Setd1a (+/-) mice. Optogenetics-assisted selective stimulation of presynaptic neurons combined with Setd1a KD reveals that Setd1a at postsynaptic site is essential for excitatory synaptic transmission. Our findings suggest that reduced SETD1A may attenuate excitatory synaptic function and contribute to the pathophysiology of SCZ.]]>
Wed, 31 Dec 1969 19:00:00 EST
Integrated Analysis of DNA Methylation, Hydroxymethylation, and Gene Expression Data Using ME-Class2. Singh MK, Edwards JR
Methods Mol Biol (2021)

There is increasing interest in understanding the pathological role of DNA methylation changes in disease by profiling genome-wide methylation changes. This includes both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). The typical profiling study is designed to measure 5mC and/or 5hmC levels alongside gene expression in a set of samples and controls to determine a list of candidate genes whose 5mC and/or 5hmC changes are associated with expression changes. We recently showed that ME-Class2 substantially outperforms other bioinformatic approaches at accurately identify genes with highly associated methylation and expression changes. ME-Class2 further illuminated how synergistic changes in 5mC and 5hmC potentially contribute to gene silencing and activation. Here we present a detailed protocol for using ME-Class2 to analyze genome-wide methylation (5mC and/or 5hmC) and expression data. Further, we provide advice about extending ME-Class2 to study the relationships between other epigenetic marks.]]>
Wed, 31 Dec 1969 19:00:00 EST
The Landscape of Genomic Imprinting at the Porcine / Locus from Methylome and Transcriptome of Parthenogenetic Embryos. Ahn J, Hwang IS, Park MR, Cho IC, Hwang S, Lee K
G3 (Bethesda) (Sep 2020)

In mammals, imprinted genes often exist in the form of clusters in specific chromosome regions. However, in pigs, genomic imprinting of a relatively few genes and clusters has been identified, and genes within or adjacent to putative imprinted clusters need to be investigated including those at the / locus. The objective of this study was to, using porcine parthenogenetic embryos, investigate imprinting status of genes within the genomic region spans between the and genes in chromosome 9. Whole-genome bisulfite sequencing (WGBS) and RNA sequencing (RNA-seq) were conducted with normal and parthenogenetic embryos, and methylome and transcriptome were analyzed. As a result, differentially methylated regions (DMRs) between the embryos were identified, and parental allele-specific expressions of the and genes were verified. The pig imprinted interval was limited between and , since both the and genes at the centromere-proximal region and the genes between and toward the telomere were non-imprinted and biallelically expressed. Consequently, our combining analyses of methylome, transcriptome, and informative polymorphisms revealed the boundary of imprinting cluster at the / locus in pig chromosome 9 and consolidated the landscape of genomic imprinting in pigs.]]>
Wed, 31 Dec 1969 19:00:00 EST
Mapping DNA Methylation in Mammals: The State of the Art. Lentini A, Nestor CE
Methods Mol Biol (2021)

A complete understanding of the dynamics and function of cytosine modifications in mammalian biology is lacking. Central to achieving this understanding is the availability of techniques that permit sensitive and specific genome-wide mapping of DNA modifications in mammalian DNA. The last decade has seen the development of a vast arsenal of novel profiling approaches enabling epigeneticists to tackle research questions that were previously out of reach. Here, we review the techniques currently available for profiling DNA modifications in mammals, discuss their strengths and weaknesses, and speculate on the future direction of DNA modification profiling technologies.]]>
Wed, 31 Dec 1969 19:00:00 EST
Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting disturbance. Cubellis MV, Pignata L, Verma A, Sparago A, Del Prete R, Monticelli M, Calzari L, Antona V, Melis D, Tenconi R, Russo S, Cerrato F, Riccio A
Clin Epigenetics (Sep 2020)

PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established.]]>
Wed, 31 Dec 1969 19:00:00 EST
Profiling Chromatin Landscape at High Resolution and Throughput with 2C-ChIP. Wang XQD, Cameron CJF, Segal D, Paquette D, Blanchette M, Dostie J
Methods Mol Biol (2021)

Chromatin immunoprecipitation (ChIP) is used to probe the presence of proteins and/or their posttranslational modifications on genomic DNA. This method is often used alongside chromosome conformation capture approaches to obtain a better-rounded view of the functional relationship between chromatin architecture and its landscape. Since the inception of ChIP, its protocol has been modified to improve speed, sensitivity, and specificity. Combining ChIP with deep sequencing has recently improved its throughput and made genome-wide profiling possible. However, genome-wide analysis is not always the best option, particularly when many samples are required to study a given genomic region or when quantitative data is desired. We recently developed carbon copy-ChIP (2C-ChIP), a new form of the high-throughput ChIP analysis method ideally suited for these types of studies. 2C-ChIP applies ligation-mediated amplification (LMA) followed by deep sequencing to quantitatively detect specified genomic regions in ChIP samples. Here, we describe the generation of 2C-ChIP libraries and computational processing of the resulting sequencing data.]]>
Wed, 31 Dec 1969 19:00:00 EST
An overview of advances in multi-omics analysis in prostate cancer. Zhang E, Zhang M, Shi C, Sun L, Shan L, Zhang H, Song Y
Life Sci (Sep 2020)

Prostate cancer (PCa) is a deadly disease for men, and studies of all types of omics data are necessary to promote precision medicine. The maturity of sequencing technology, the improvements of computer processing power, and the progress achieved in omics analysis methods have improved research efficiency and saved research costs. The occurrence and development of PCa is due to multisystem and multilevel pathological changes. Although omics research at a single level is important, this approach often has limitations. In contrast, the combined analysis of multiple types of omics data can better analyze PCa changes as a whole, thus ensuring the validity of research results to the greatest extent. This paper introduces the applications of single omics in PCa and then summarizes research progress in the combined analysis of two or more types of omics data, so as to systematically and comprehensively analyze the necessity of combined analysis of multiple omics data in PCa.]]>
Wed, 31 Dec 1969 19:00:00 EST
GENETICS IN ENDOCRINOLOGY: Genetic etiologies of central precocious puberty and the role of imprinted genes. Roberts SA, Kaiser UB
Eur J Endocrinol (Oct 2020)

Pubertal timing is regulated by the complex interplay of genetic, environmental, nutritional and epigenetic factors. Criteria for determining normal pubertal timing, and thus the definition of precocious puberty, have evolved based on published population studies. The significance of the genetic influence on pubertal timing is supported by familial pubertal timing and twin studies. In contrast to the many monogenic causes associated with hypogonadotropic hypogonadism, only four monogenic causes of central precocious puberty (CPP) have been described. Loss-of-function mutations in Makorin Ring Finger Protein 3(MKRN3), a maternally imprinted gene on chromosome 15 within the Prader-Willi syndrome locus, are the most common identified genetic cause of CPP. More recently, several mutations in a second maternally imprinted gene, Delta-like noncanonical Notch ligand 1 (DLK1), have also been associated with CPP. Polymorphisms in both genes have also been associated with the age of menarche in genome-wide association studies. Mutations in the genes encoding kisspeptin (KISS1) and its receptor (KISS1R), potent activators of GnRH secretion, have also been described in association with CPP, but remain rare monogenic causes. CPP has both short- and long-term health implications for children, highlighting the importance of understanding the mechanisms contributing to early puberty. Additionally, given the role of mutations in the imprinted genes MKRN3 and DLK1 in pubertal timing, other imprinted candidate genes should be considered for a role in puberty initiation.]]>
Wed, 31 Dec 1969 19:00:00 EST
Epigenetic Assays in Purified Cardiomyocyte Nuclei. Hill MC, Martin JF
Methods Mol Biol (2021)

The adult mammalian heart's potential for regeneration is very inefficient. Importantly, adult mammalian cardiomyocytes (CMs) are characterized as a cell population with very limited mitotic potential. Conversely, the neonatal mouse heart possesses a brief, yet robust, regenerative capacity within the first week of life. Cell type-specific enrichment procedures are essential for characterizing the full spectrum of epigenomic landscapes and gene regulatory networks deployed by mammalian CMs. In this chapter, we describe a protocol useful for purifying CM nuclei from mammalian cardiac tissue. Furthermore, we detail a low-input procedure suitable for the parallel genome-wide profiling of chromatin accessibility, histone modifications, and transcription factor-binding sites. The CM nuclei purified using this process are suitable for multi-omic profiling approaches.]]>
Wed, 31 Dec 1969 19:00:00 EST
Aberrant allelic-switch of antisense lncRNA IRAIN may be an early diagnostic marker in laryngeal cancer. Wang JY, Liu D, Di Meng Y, Guo YY, Zhao M
Oncol Lett (Oct 2020)

Laryngeal carcinoma is a common head and neck malignancy, however, the molecular mechanism of the disease has not yet been elucidated. The present study aimed to investigate the role of IGF1R antisense imprinted non-protein coding RNA (IRAIN) long non-coding (lnc)RNA in laryngeal carcinoma. In total, specimens of healthy pharynx tissue from 6 healthy individuals, carcinoma tissue and paracancerous tissue from 37 patients with laryngeal carcinoma were used in this study. The single nucleotide polymorphism (SNP) rs8034564 was used to distinguish the two parental alleles of IRAIN. DNA and RNA were extracted from tissue specimens and the IRAIN allelic gene was sequenced. Reverse transcription-quantitative PCR was used to determine the expression levels of IRAIN and Insulin-like growth factor 1 receptor (IGF1R) in laryngeal carcinoma and paracancerous tissue. Bisulfite genomic sequencing was used to determine IRAIN promoter DNA methylation status in laryngeal carcinoma tissue. The expression of IRAIN was di-allelic in healthy pharynx tissue, laryngeal carcinoma tissue and paracancerous tissue. Moreover, IRAIN expression in laryngeal carcinoma tissue was lower compared with paracancerous tissue (P<0.05). IRAIN expression was not associated with age, histological type, tumor stage and grade and lymph node metastasis. IRAIN allelic expression imbalance was present in laryngeal carcinoma and paracancerous tissue, but not in healthy pharynx tissue. SNP analysis (rs8034564) indicated there was an allelic-switch of the two parental alleles. Furthermore, epigenetic analysis revealed no extensive DNA methylation of CpG islands in the IRAIN gene promoter of laryngeal carcinoma. Therefore, it was suggested that IRAIN allele was non-imprinted in laryngeal carcinoma and healthy pharynx tissue. It was also demonstrated that IRAIN may be a potential tumor suppressor in laryngeal carcinoma, and that DNA methylation is not involved in the regulation of IRAIN gene immobilization in laryngeal carcinoma tissue. Thus, detection of IRAIN allelic expression imbalance and aberrant allele-switch may serve as an early diagnostic marker of laryngeal carcinoma.]]>
Wed, 31 Dec 1969 19:00:00 EST
Immunogenomic Landscape of Hematological Malignancies. Dufva O, Pölönen P, Brück O, Keränen MAI, Klievink J, Mehtonen J, Huuhtanen J, Kumar A, Malani D, Siitonen S, Kankainen M, Ghimire B, Lahtela J, Mattila P, Vähä-Koskela M, Wennerberg K, Granberg K, Leivonen SK, Meriranta L, Heckman C, Leppä S, Nykter M, Lohi O, Heinäniemi M, Mustjoki S
Cancer Cell (Sep 2020)

Understanding factors that shape the immune landscape across hematological malignancies is essential for immunotherapy development. We integrated over 8,000 transcriptomes and 2,000 samples with multilevel genomics of hematological cancers to investigate how immunological features are linked to cancer subtypes, genetic and epigenetic alterations, and patient survival, and validated key findings experimentally. Infiltration of cytotoxic lymphocytes was associated with TP53 and myelodysplasia-related changes in acute myeloid leukemia, and activated B cell-like phenotype and interferon-γ response in lymphoma. CIITA methylation regulating antigen presentation, cancer type-specific immune checkpoints, such as VISTA in myeloid malignancies, and variation in cancer antigen expression further contributed to immune heterogeneity and predicted survival. Our study provides a resource linking immunology with cancer subtypes and genomics in hematological malignancies.]]>
Wed, 31 Dec 1969 19:00:00 EST
Longitudinal Characteristics of Glioblastoma in Genome-Wide Studies. Kraboth Z, Kalman B
Pathol Oncol Res (Oct 2020)

Glioblastoma is one of the deadliest tumors with barely over one-year median survival despite intensive efforts in defining its molecular characteristics and searching for innovative treatment strategies. While major progress has been made in cataloging cross-sectional genomic, transcriptomic and epigenomic features of the tumor, and inferring its main molecular pathways and niches for potential targeted intervention, we still do not have sufficient knowledge concerning evolutionary patterns and dynamics of molecular changes or the treatment-induced effects affecting glioblastoma biology. In this review, we summarize the results of recent longitudinal genomic, transcriptomic and epigenomic studies that brought us closer to a better understanding of this lethal disease. Evidence suggests that neuronal / glioma stem cells with accumulating mutations initiate glioblastoma development and recurrence, but the hypothetical models describing the courses that lead to established tumors have not been fully proven. Moving from the histopathological phenotype to the results of high resolution OMICS studies, we try to synthesize the currently available information from sequential glioblastoma analyses in order to highlight its multifaceted features and heterogenetity, as well as the expected complexity of potential treatment strategies that might once succeed.]]>
Wed, 31 Dec 1969 19:00:00 EST
Polyploidy of semi-cloned embryos generated from parthenogenetic haploid embryonic stem cells. Aizawa E, Dumeau CE, Freimann R, Di Minin G, Wutz A
PLoS One (2020)

In mammals, the fusion of two gametes, an oocyte and a spermatozoon, during fertilization forms a totipotent zygote. There has been no reported case of adult mammal development by natural parthenogenesis, in which embryos develop from unfertilized oocytes. The genome and epigenetic information of haploid gametes are crucial for mammalian development. Haploid embryonic stem cells (haESCs) can be established from uniparental blastocysts and possess only one set of chromosomes. Previous studies have shown that sperm or oocyte genome can be replaced by haESCs with or without manipulation of genomic imprinting for generation of mice. Recently, these remarkable semi-cloning methods have been applied for screening of key factors of mouse embryonic development. While haESCs have been applied as substitutes of gametic genomes, the fundamental mechanism how haESCs contribute to the genome of totipotent embryos is unclear. Here, we show the generation of fertile semi-cloned mice by injection of parthenogenetic haESCs (phaESCs) into oocytes after deletion of two differentially methylated regions (DMRs), the IG-DMR and H19-DMR. For characterizing the genome of semi-cloned embryos further, we establish ESC lines from semi-cloned blastocysts. We report that polyploid karyotypes are observed in semi-cloned ESCs (scESCs). Our results confirm that mitotically arrested phaESCs yield semi-cloned embryos and mice when the IG-DMR and H19-DMR are deleted. In addition, we highlight the occurrence of polyploidy that needs to be considered for further improving the development of semi-cloned embryos derived by haESC injection.]]>
Wed, 31 Dec 1969 19:00:00 EST
Histone Modifications and their Role in Colorectal Cancer (Review). Qin J, Wen B, Liang Y, Yu W, Li H
Pathol Oncol Res (Oct 2020)

The development of colorectal cancer is a complex and multistep process mediated by a variety of factors including the dysregulation of genetic and epigenetic under the influence of microenvironment. It is evident that epigenetics that affects gene activity and expression has been recognized as a critical role in the carcinogenesis. Aside from DNA methylation, miRNA level, and genomic imprinting, histone modification is increasingly recognized as an essential mechanism underlying the occurrence and development of colorectal cancer. Aberrant regulation of histone modification like acetylation, methylation and phosphorylation levels on specific residues is implicated in a wide spectrum of cancers, including colorectal cancer. In addition, as this process is reversible and accompanied by a plethora of deregulated enzymes, inhibiting those histone-modifying enzymes activity and regulating its level has been thought of as a potential path for tumor therapy. This review provides insight into the basic information of histone modification and its application in the colorectal cancer treatment, thereby offering new potential targets for treatment of colorectal cancer.]]>
Wed, 31 Dec 1969 19:00:00 EST
Global DNA methylation in placental tissues from pregnant with preeclampsia: A systematic review and pathway analysis. Cruz JO, Conceição IMCA, Tosatti JAG, Gomes KB, Luizon MR
Placenta (Sep 2020)

Pre-eclampsia (PE) is the major cause of fetal and maternal mortality and can be classified according to gestational age of onset into early-onset (EOPE, <34 weeks of gestation) and late- (LOPE, ≥34 weeks of gestation). DNA methylation (DNAm) may help to understand the abnormal placentation in PE. Therefore, we performed a systematic review to assess the role of global DNAm on pathophysiology of PE, focused on fetal and maternal tissues of placenta from pregnant with PE, including EOPE and LOPE. We searched the databases EMBASE, Medline/PubMed, Cochrane Central Register of Controlled Trials, Scopus, Lilacs, Scielo and Google Scholar, and followed the MOOSE guidelines. Moreover, we performed pathway analysis with the overlapping genes from the included studies. Twelve out of 24 included studies in the qualitative analysis considered the classification into EOPE and LOPE. We did not found heterogeneity in the criteria used for diagnosis of PE, and a few studies evaluated whether confounding factors would influence placental DNAm. Fourteen out of 24 included studies showed hypomethylation in placental tissue from pregnant with PE compared to controls. The differences in DNAm are specific to genes or differentially methylated regions, and more evident in EOPE and preterm PE compared to controls, rather than LOPE and term PE. The overlapping genes from included studies revealed pathways relevant to pathophysiology of PE. Our findings highlighted the heterogeneous results of the included studies, mainly focused on North America and China. Replication studies in different populations should use the same placental tissues, techniques to assess DNAm and pipelines for bioinformatic analysis.]]>
Wed, 31 Dec 1969 19:00:00 EST
Impact of parental origin of X-chromosome on clinical and biochemical profile in Turner syndrome. Malhotra R, Shukla R, Kabra M, Gupta Y, Jyotsna VP, Khadgawat R
J Pediatr Endocrinol Metab (Sep 2020)

Objectives To evaluate if the parental origin of X-chromosome has an impact on the phenotype and biochemical profile in Turner syndrome (TS). Result of the previous studies have been equivocal and could be attributable to the multicentric study design with different experts examining heterogeneous TS population of various ethnic background. Methods A cross-sectional single center study from Northern India. Fifty nine diagnosed subjects of TS and their parents participated in the study. Parental origin of intact X-chromosome was determined using 12 highly polymorphic short tandem repeats (STR) on X-chromosome. For the evaluation of parent-of-origin effects, typical phenotypic traits including congenital malformations, anthropometry, body composition by dual energy X-ray absorptiometry (DXA) and biochemical profile were compared. Clinical stigmata of TS in all subjects were examined by a single expert. Results The intact X-chromosome was of maternal origin (Xm) in 49.1% subjects while 50.9% had paternal origin (Xp). Skeletal anomalies were more common in Xm group, out of which prevalence of short neck and short fourth metatarsal reached statistical significance (p=0.04 and 0.01 respectively). A strong correlation was observed between subject's baseline height standard deviation score (Ht SDS) and paternal height (r=0.593, p<0.001), maternal height (r=0.564, p<0.001) and mid-parental height (MPH) (r=0.372, p=0.047) in Xp group. This effect was not seen in Xm subjects whose baseline Ht SDS showed no significant correlation with maternal height, paternal height or MPH. No differences were detected between the groups with regard to biochemical profile or body composition. Conclusions We speculate that the differences in skeletal anomalies and height correlations between Xm and Xp groups could be due to the modifying effect of epigenetic signature on short stature homeobox (SHOX) gene of Xm. SHOX gene is not modified on Xp thereby explaining the paucity of skeletal changes and height correlations in Xp subjects.]]>
Wed, 31 Dec 1969 19:00:00 EST
Deficiency and overexpression of in the mouse cause distinct muscle abnormalities related to Temple and Kagami-Ogata syndromes. Kitazawa M, Hayashi S, Imamura M, Takeda S, Oishi Y, Kaneko-Ishino T, Ishino F
Development (Sep 2020)

Temple and Kagami-Ogata syndromes are genomic imprinting diseases caused by maternal and paternal duplication of human chromosome 14, respectively. They exhibit different postnatal muscle-related symptoms as well as prenatal placental problems. Using the mouse models for these syndromes, it has been demonstrated that retrotransposon gag like 1 [, also known as paternally expressed 11 ()] located in the mouse orthologous imprinted region is responsible for the prenatal placental problems because it is an essential placental gene for maintenance of fetal capillary network during gestation. However, the causative imprinted gene for the postnatal muscle-related symptoms remains unknown. Here, we demonstrate that also plays an important role in fetal/neonatal skeletal muscle development: its deletion and overproduction in mice lead to neonatal lethality associated with severe but distinct skeletal muscle defects, similar to those of Temple and Kagami-Ogata syndromes, respectively. Thus, it is strongly suggested that is the major gene responsible for the muscle defects in addition to the placental defects in these two genomic imprinting diseases. This is the first example of an LTR retrotransposon-derived gene specific to eutherians contributing to eutherian skeletal muscle development.]]>
Wed, 31 Dec 1969 19:00:00 EST
Biallelic variant in cyclin B3 is associated with failure of maternal meiosis II and recurrent digynic triploidy. Fatemi N, Salehi N, Pignata L, Palumbo P, Cubellis MV, Ramazanali F, Ray P, Varkiani M, Reyhani-Sabet F, Biglari A, Sparago A, Acurzio B, Palumbo O, Carella M, Riccio A, Totonchi M
J Med Genet (Sep 2020)

Triploidy is one of the most common chromosome abnormalities affecting human gestation and accounts for an important fraction of first-trimester miscarriages. Triploidy has been demonstrated in a few cases of recurrent pregnancy loss (RPL) but its molecular mechanisms are unknown. This study aims to identify the genetic cause of RPL associated with fetus triploidy.]]>
Wed, 31 Dec 1969 19:00:00 EST
Single-cell sequencing of miRNAs: A modified technology. Chakraborty C, Bhattacharya M, Agoramoorthy G
Cell Biol Int (Sep 2020)

The recent development of next-generation sequencing technologies has offered valuable insights into individual cells. This technology is centered on the characterization of single cells for epigenomics, genomics, and transcriptomics. Ever since the first report appeared in 2009, the single-cell RNA-sequencing saga started to explore deeper into the mechanics intrigued within a single cell. microRNA (miRNA) has been increasingly recognized as an essential molecule triggering an additional layer for gene regulation. Therefore, single-cell sequencing of miRNAs is crucial to explore the logical riddles surrounding the epigenomics, genomics, and transcriptomics of an individual cell. Scientists from the Vienna Biocenter Campus have lately performed single-cell sequencing of miRNAs in the fly, Drosophila, and nematode, Caenorhabditis elegans. In this review, we present the latest scientific explorations supported by all-inclusive data on this novel subject matter of next-generation sequencing.]]>
Wed, 31 Dec 1969 19:00:00 EST