Imprinted genes and regulation of gene expression by epigenetic inheritance

1996 ◽  
Vol 8 (3) ◽  
pp. 348-353 ◽  
Author(s):  
Rosalind M John ◽  
M Azim Surani
2004 ◽  
Vol 3 (3) ◽  
pp. 8-17
Author(s):  
S. A. Nazarenko

Genomic imprinting is a form of non-Mendelian epigenetic inheritance that is defined by differential gene expression depending on its parental origin — maternal or paternal. It is known about 60 imprinted genes many of which effect significantly on the fetus growth and development. Methylation of DNA cytosine bases that defines the interaction of DNA and proteins identifying the modified bases and controls the gene expression through chromatin compacting-decompacting mechanism, is a main epigenetic genom modifier. Disturbances in monoallelic gene expression lead to the development of a special class of human hereditary diseases — genomic imprinting diseases.


Author(s):  
Eva Jablonka ◽  
Zohar Bronfman

Behavioral epigenetics is part of the thriving field of epigenetics, which describes the study of developmental processes that lead to persistent changes in the states of organisms, their components, and their lineages. Such developmental, context-sensitive changes are mediated by epigenetic mechanisms that establish and maintain the changes in patterns of gene expression and cellular structures that occur during ontogeny in both nondividing cells, such as most mature neurons, and dividing cells such as stem cells. When information is vertically transmitted to cells during cell division, or horizontally between cells through migrating reproducing molecules (like small RNAs), and when variations in the transmitted information are not determined by variations in DNA sequence (i.e., the same DNA sequence has more than one cell-heritable epigenetic state), epigenetic inheritance is said to occur. Behavioral epigenetics investigates the role of behavior in the shaping of developmental epigenetic states and the reciprocal role of epigenetic factors and mechanisms in the shaping of the behavior of human and nonhuman animals, at the short-, middle-, and long-term (ontogenetic, ecological, and evolutionary) time scales. The focus is on the molecular-epigenetic study of the interactions between environmental factors, such as ecological factors and habitual activities such as lifestyles and learning, with genetic variation and the neurobiological and physiological mechanisms that mediate between the regulation of gene expression and behavior. This range of epigenetic processes therefore includes, but is not limited to, studies involving epigenetic inheritance and the direct and indirect evolutionary effects of epigenetic developmental mechanisms. The neural-behavioral aspects that occur during ontogeny through the mediation of epigenetic mechanisms are central to behavioral epigenetics and are the main focus of neural epigenetics.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Liyun Yuan ◽  
Xiaoyan Tang ◽  
Binyan Zhang ◽  
Guohui Ding

Pluripotent stem cells are exhibited similarly in the morphology, gene expression, growth properties, and epigenetic modification with embryonic stem cells (ESCs). However, it is still controversial that the pluripotency of induced pluripotent stem cell (iPSC) is much inferior to ESC, and the differentiation capacity of iPSC and ESC can also be separated by transcriptome and epigenetics. miRNAs, which act in posttranscriptional regulation of gene expression and are involved in many basic cellular processes, may reveal the answer. In this paper, we focused on identifying the hidden relationship between miRNAs and imprinted genes in cell pluripotency. Total miRNA expression patterns in iPSC and ES cells were comprehensively analysed and linked with human imprinted genes, which show a global picture of their potential function in pluripotent level. A new CPA4-KLF14 region which locates in chromosomal homologous segments (CHSs) within mammals and include both imprinted genes and significantly expressed miRNAs was first identified. Molecular network analysis showed genes interacted with imprinted genes closely and enriched in modules such as cancer, cell death and survival, and tumor morphology. This imprinted region may provide a new look for those who are interested in cell pluripotency of hiPSCs and hESCs.


2020 ◽  
Vol 477 (16) ◽  
pp. 3091-3104 ◽  
Author(s):  
Luciana E. Giono ◽  
Alberto R. Kornblihtt

Gene expression is an intricately regulated process that is at the basis of cell differentiation, the maintenance of cell identity and the cellular responses to environmental changes. Alternative splicing, the process by which multiple functionally distinct transcripts are generated from a single gene, is one of the main mechanisms that contribute to expand the coding capacity of genomes and help explain the level of complexity achieved by higher organisms. Eukaryotic transcription is subject to multiple layers of regulation both intrinsic — such as promoter structure — and dynamic, allowing the cell to respond to internal and external signals. Similarly, alternative splicing choices are affected by all of these aspects, mainly through the regulation of transcription elongation, making it a regulatory knob on a par with the regulation of gene expression levels. This review aims to recapitulate some of the history and stepping-stones that led to the paradigms held today about transcription and splicing regulation, with major focus on transcription elongation and its effect on alternative splicing.


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