Journal of Clinical Epigenetics Open Access

Reproductive Technologies Involved In Imprinting Epigenetics

Alain Robbe^* Department of Clinical Epigenetics, University of Antwerp, Belgium
^*Correspondence: Alain Robbe, Department of Clinical Epigenetics, University of Antwerp, Belgium, Email:

Received: 04-May-2022, Manuscript No. IPJCE-22-13480; Editor assigned: 06-May-2022, Pre QC No. IPJCE-22-13480 (PQ); Reviewed: 20-May-2022, QC No. IPJCE-22-13480; Revised: 24-May-2022, Manuscript No. IPJCE-22-13480 (R); Published: 01-Jun-2022, DOI: 10.21767/2472-1158-22.8.23

Introduction

This review describes the importance of genetic and epigenetic factors in the pathophysiology of male infertility. Interactions between thousands of genes, epigenetic regulation of gene expression, and environmental and lifestyle factors that affect genetic and epigenetic variants determine the resulting male infertility phenotype. Currently, karyotype analysis, y chromosome micro deletion screening, and CFTR gene mutation testing are routinely performed to investigate possible genetic etiology in patients with azoospermia and severe oligospermia.

Description

As tissue macrophages in the central nervous system (CNS), microglia forms the central immune cells of this organ. The properties of microglia are highly dependent on environmental cues such as the symbiotic microbial flora. Gut microbiota are known to continuously regulate the maturation and function of microglia through the production of short-chain fatty acids (SCFAs). However, the exact mechanism of this crosstalk is unknown. Here, the immature phenotype of sterile (GF) mouse microglia is epigenically imprinted by H3K4me3 and H3K9ac on metabolic genes associated with major functional changes such as increased mitochondrial mass and specific respiratory chain dysfunction.

The purpose of this review is to critically consider the data that supports the programming concepts and their implications. Birth weight and growth trajectory in childhood are associated with cardiometabolic disorders in adulthood. Both extreme birth weight and birth weight, coupled with postnatal growth, increase the early presence of cardiometabolic risk factors and vascular imprinting, which are key components of this framework. Data from epigenetics, proteomics, metabolomics, and microbiota added relevant information and helped develop biomarkers that not only helped to better understand the mechanism, but also helped to take action.

Human glioblastoma (GBM) describes the existence of a small population of cells with stem cell properties called glioma stem cells (GSC). These cells may be GBM and are involved in tumor development. However, it has not yet been determined whether GSC is derived from normal neural stem cells (NSCs) as a result of genetic and epigenetic alterations and/or somatic cell dedifferentiation. Genomic imprinting is an epigenetic marking process that expresses genes according to their parental origin. Imprinting pattern dysregulation or loss of genomic imprinting (LOI) has been reported in a variety of tumors, including GBM, and is one of the earliest and most common events that occur in human cancers.

In vitro fertilization and somatic cell nuclear transfer are assisted reproductive technologies commonly used in humans and cattle, respectively. Despite these technological advances, molecular errors can occur that increase the likelihood of imprinting defects in the offspring. Large progeny syndrome/abnormal progeny syndrome has been reported in cattle and is characterized by overgrowth, organ malformations, skeletal and placental defects. In humans, Beckwith-Wiedemann Syndrome (BWS) exhibits phenotypic characteristics similar to LOS/AOS. In both syndromes, disruption of genomic imprinting, coupled with parent-specific expression and loss of parent-specific epigenetic marks, is associated with molecular etiology.

Conclusion

Genomic imprinting is an epigenetic phenomenon that causes biased expression of maternal and paternal hereditary alleles. In flowering plants, genomic imprinting occurs primarily in triploid endosperm and plays an important role in seed development. In this study, a deep RNA sequence was used to 248 candidate ins containing 114 maternally expressed imprint genes (MEGs) and 134 paternally expressed imprint genes (PEGs) in flax (Linum usitatissimum L) embryos. These imprinted genes were not clustered in specific chromosomal regions and were not well conserved in flax and other plant species.