AI Article Synopsis
- All mammalian somatic cells come from a single fertilized cell (the zygote) and have identical genetic information, despite experiencing significant changes during development.
- Epigenetic modifications play a crucial role in determining and maintaining specific gene expression patterns as cells differentiate.
- Advances in research show that it's possible to erase and change the identity of cells, even reprogramming differentiated cells back to a pluripotent state, thanks to transcription factors and epigenetic modifiers.
Article Abstract
All mammalian somatic cells originate from a single fertilized cell, the zygote, and share identical genetic information despite the dramatic changes in cell structure and function that accompany organismal development. The genome is subjected to a wide array of epigenetic modifications during lineage specification, a process that contributes to the implementation and maintenance of specific gene expression programs in somatic cells. Nuclear transfer and cell-fusion experiments demonstrate that the epigenetic signature directing a cell identity can be erased and modified into that of another cell type. Furthermore, in the case of cloning, differentiated cells can be reprogrammed back to pluripotency to support the reexpression of all developmental programs. Recent breakthroughs highlight the importance of transcription factors as well as epigenetic modifiers in the establishment, maintenance, and rewiring of cell identity. By focusing on reprogramming of terminally differentiated lymphocytes, we review and highlight recent insights into the molecular mechanisms and cellular events potentially underlying programming and reprogramming of somatic cell identity in mammals.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1101/sqb.2008.73.025 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Chronic nicotine exposure induces molecular and transcriptomic endophenotypes associated with mood and anxiety disorders in a cerebral organoid neurodevelopmental model.
Front Pharmacol
December 2024
Addiction Research Group, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Introduction: Prenatal nicotine exposure (PNE) from maternal smoking disrupts regulatory processes vital to fetal development. These changes result in long-term behavioral impairments, including mood and anxiety disorders, that manifest later in life. However, the relationship underlying PNE, and the underpinnings of mood and anxiety molecular and transcriptomic phenotypes remains elusive.
View Article and Find Full Text PDFRecent studies indicate that the development of drug resistance and increased invasiveness in melanoma is largely driven by transcriptional plasticity rather than canonical coding mutations. Understanding the mechanisms behind cell identity shifts in oncogenic transformation and cancer progression is crucial for advancing our understanding of melanoma and other aggressive cancers. While distinct melanoma phenotypic states have been well characterized, the processes and transcriptional controls that enable cells to shift between these states remain largely unknown.
View Article and Find Full Text PDFWithin cells multiple related transcription factors targeting the same sequences may co-exist, leading to potential regulatory cooperativity, redundancy or competition. Yet the differential roles and biological functions of co-targeting transcription factors is poorly understood. In melanoma, three highly-related transcription factors are co-expressed: The mTORC1-regulated TFEB and TFE3, that are key effectors of a wide range of metabolic and microenvironmental cues; and MITF, that controls melanoma phenotypic identity.
View Article and Find Full Text PDFIt is becoming more broadly accepted that human-based models are needed to better understand the complexities of the human nervous system and its diseases. The recently developed human brain organotypic culture model is one highly promising model that requires the involvement of neurosurgeons and neurosurgical patients. Studies have investigated the electrophysiological properties of neurons in such human tissues, but the maintenance of other cell types within explanted brain remains largely unknown.
View Article and Find Full Text PDFTraumatic brain injury (TBI) is a leading cause of mortality and disability worldwide and can lead to secondary sequelae such as increased seizure susceptibility. Emerging work suggests that the thalamus, the relay center of the brain that undergoes secondary damage after cortical TBI, is involved with heightened seizure risks after TBI. TBI also induces the recruitment of peripheral immune cells, including T cells, to the site(s) of injury, but it is unclear how these cells impact neurological sequelae post-TBI.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!