Determination of cell fate selection during phage lambda infection

Notch is involved in the cell fate determination of many cell lineages. The intracellular region (RAMIC) of Notch1 transactivates genes by interaction with a DNA binding protein RBP-J. We have compared the activities of mouse RAMIC and its derivatives in transactivation and differentiation suppression of myogenic precursor cells. RAMIC comprises two separate domains, IC for transactivation and RAM for RBP-J binding. Although the physical interaction of IC with RBP-J was much weaker than with RAM, transactivation activity of IC was shown to involve RBP-J by using an RBP-J null mutant cell line. IC showed differentiation suppression activity that was generally comparable to its transactivation activity. The RBP-J-VP16 fusion protein, which has strong transactivation activity, also suppressed myogenesis of C2C12. The RAM domain, which has no other activities than binding to RBP-J, synergistically stimulated transactivation activity of IC to the level of RAMIC. The RAM domain was proposed to compete with a putative co-repressor for binding to RBP-J because the RAM domain can also stimulate the activity of RBP-J-VP16. These results taken together, indicate that differentiation suppression of myogenic precursor cells by Notch signalling is due to transactivation of genes carrying RBP-J binding motifs.

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Hypoxia in Cell Reprogramming and the Epigenetic Regulations

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.609984 ◽

2021 ◽

Vol 9 ◽

Author(s):

Nariaki Nakamura ◽

Xiaobing Shi ◽

Radbod Darabi ◽

Yong Li

Keyword(s):

Cell Proliferation ◽

Cell Fate ◽

Tissue Regeneration ◽

Cellular Reprogramming ◽

Cell Reprogramming ◽

Cell Renewal ◽

Cellular Functions ◽

Stem Cell Renewal ◽

Epigenetic Regulations

Cellular reprogramming is a fundamental topic in the research of stem cells and molecular biology. It is widely investigated and its understanding is crucial for learning about different aspects of development such as cell proliferation, determination of cell fate and stem cell renewal. Other factors involved during development include hypoxia and epigenetics, which play major roles in the development of tissues and organs. This review will discuss the involvement of hypoxia and epigenetics in the regulation of cellular reprogramming and how interplay between each factor can contribute to different cellular functions as well as tissue regeneration.

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Topical Review: Cortical Malformation and Pediatric Epilepsy: A Molecular Genetic Approach

Journal of Child Neurology ◽

10.1177/08830738040190030501 ◽

2004 ◽

Vol 19 (3) ◽

pp. 300-303

Author(s):

Ganeshwaran H. Mochida

Keyword(s):

Human Brain ◽

Cell Fate ◽

Molecular Genetic ◽

Pediatric Epilepsy ◽

Causative Gene ◽

Cortical Malformation ◽

Neuronal Progenitor ◽

Cortical Patterning ◽

Low Incidence

Genetic malformations of the cerebral cortex are important causes of neurologic morbidity in children because they are often associated with developmental delay, motor disturbances (cerebral palsy), and epilepsy. Primary autosomal recessive microcephaly is a cortical malformation with a low incidence of epilepsy. One of its causative genes, ASPM, might play an important role in regulating proliferation of neuronal progenitor cells. Mutations in ASPM do not seem to affect later stages of cortical development, such as neuronal migration, and this might be responsible for the low epileptogenicity of this malformation. ASPM might also have played an important role in the evolutionary expansion of the human brain. Bilateral frontoparietal polymicrogyria, on the other hand, is a highly epileptogenic malformation. Its causative gene, GPR56 , is also expressed in the neurogenic regions of the cortex, but its primary function might be in the determination of cell fate and/or cortical patterning. Further studies of these genes will likely lead to a better understanding of human brain development and epilepsy. ( J Child Neurol 2005;20:300—303).

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N6-Methyladenosine in RNA and DNA: An Epitranscriptomic and Epigenetic Player Implicated in Determination of Stem Cell Fate

Stem Cells International ◽

10.1155/2018/3256524 ◽

2018 ◽

Vol 2018 ◽

pp. 1-18 ◽

Cited By ~ 16

Author(s):

Pengfei Ji ◽

Xia Wang ◽

Nina Xie ◽

Yujing Li

Keyword(s):

Stem Cells ◽

Stem Cell ◽

Cell Fate ◽

Direct Interaction ◽

Limited Information ◽

Stem Cell Fate ◽

Base Modification ◽

Dna And Rna ◽

Proliferation And Differentiation

Vast emerging evidences are linking the base modifications and determination of stem cell fate such as proliferation and differentiation. Among the base modification markers extensively studied, 5-methylcytosine (5-mC) and its oxidative derivatives (5-hydroxymethylcytosine (5-hmC), 5-formylcytosine (5-fC), and 5-carboxylcytosine (5-caC)) dynamically occur in DNA and RNA and have been acknowledged as important epigenetic markers involved in regulation of cellular biological processes. N6-Methyladenosine modification in DNA (m6dA), mRNA (m6A), tRNA, and other noncoding RNAs has been defined as another important epigenetic and epitranscriptomic marker in eukaryotes in recent years. The mRNA m6A modification has been characterized biochemically, molecularly, and phenotypically, including elucidation of its methyltransferase complexes (m6A writer), demethylases (m6A eraser), and direct interaction proteins (readers), while limited information on the DNA m6dA is available. The levels and the landscapes of m6A in the epitranscriptomes and epigenomes are precisely and dynamically regulated by the fine-tuned coordination of the writers and erasers in accordance with stages of the growth, development, and reproduction as naturally programmed during the lifespan. Additionally, progress has been made in appreciation of the link between aberrant m6A modification in stem cells and diseases, like cancers and neurodegenerative disorders. These achievements are inspiring scientists to further uncover the epigenetic mechanisms for stem cell development and to dissect pathogenesis of the multiple diseases conferred by development aberration of the stem cells. This review article will highlight the research advances in the role of m6A methylation modifications of DNA and RNA in the regulation of stem cell and genesis of the closely related disorders. Additionally, this article will also address the research directions in the future.

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Following Cell-fate in E. coli After Infection by Phage Lambda

Journal of Visualized Experiments ◽

10.3791/3363 ◽

2011 ◽

Cited By ~ 6

Author(s):

Lanying Zeng ◽

Ido Golding

Keyword(s):

Cell Fate ◽

Phage Lambda ◽

E Coli

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Analysis of the myogenin promoter reveals an indirect pathway for positive autoregulation mediated by the muscle-specific enhancer factor MEF-2.

Molecular and Cellular Biology ◽

10.1128/mcb.12.9.3665 ◽

1992 ◽

Vol 12 (9) ◽

pp. 3665-3677 ◽

Cited By ~ 193

Author(s):

D G Edmondson ◽

T C Cheng ◽

P Cserjesi ◽

T Chakraborty ◽

E N Olson

Keyword(s):

Cell Fate ◽

Consensus Sequence ◽

Cell Lineage ◽

Mammalian Development ◽

Indirect Pathway ◽

Binding Factor ◽

Nonmuscle Cells ◽

And Function ◽

Myod Gene

Transcriptional cascades that specify cell fate have been well described in invertebrates. In mammalian development, however, gene hierarchies involved in determination of cell lineage are not understood. With the recent cloning of the MyoD family of myogenic regulatory factors, a model system has become available with which to study the dynamics of muscle determination in mammalian development. Myogenin, along with other members of the MyoD gene family, possesses the apparent ability to redirect nonmuscle cells into the myogenic lineage. This ability appears to be due to the direct activation of an array of subordinate or downstream genes which are responsible for formation and function of the muscle contractile apparatus. Myogenin-directed transcription has been shown to occur through interaction with a DNA consensus sequence known as an E box (CANNTG) present in the control regions of numerous downstream genes. In addition to activating the transcription of subordinate genes, members of the MyoD family positively regulate their own expression and cross-activate one another's expression. These autoregulatory interactions have been suggested as a mechanism for induction and maintenance of the myogenic phenotype, but the molecular details of the autoregulatory circuits are undefined. Here we show that the myogenin promoter contains a binding site for the myocyte-specific enhancer-binding factor, MEF-2, which can function as an intermediary of myogenin autoactivation. Since MEF-2 can be induced by myogenin, these results suggest that myogenin and MEF-2 participate in a transcriptional cascade in which MEF-2, once induced by myogenin, acts to amplify and maintain the myogenic phenotype by acting as a positive regulator of myogenin expression.

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