Related Experiment Video
Updated: Aug 29, 2025
07:46
Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos
Published on: June 23, 2023
2.7K
ASH1L contributes to oocyte apoptosis by regulating DNA damage
Tuo Zhang1,2,3, Tianhe Ren1, Huan Lin1
1Transformation Engineering Research Center of Chronic Disease Diagnosis and Treatment, Department of Physiology, College of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou Province, China.
American Journal of Physiology. Cell Physiology
|September 12, 2022
Summary
ASH1-like histone lysine methyltransferase (ASH1L) controls fetal oocyte apoptosis during meiosis. Overexpression of Ash1l reduces the primordial follicle pool, impacting female fertility.
Area of Science:
- Reproductive Biology
- Epigenetics
- Developmental Biology
Background:
- The primordial follicle pool size dictates female reproductive lifespan.
- Oocyte loss during fetal development is programmed but poorly understood.
Purpose of the Study:
- To investigate the role of ASH1-like histone lysine methyltransferase (ASH1L) in fetal oocyte apoptosis and primordial follicle pool establishment.
- To elucidate the mechanism by which ASH1L influences oocyte genome integrity.
Main Methods:
- Overexpression of Ash1l in fetal mouse ovaries.
- Assessment of oocyte apoptosis via TUNEL assay.
- Analysis of DNA double-strand break repair markers (e.g., p63, p-CHK2).
Main Results:
- Overexpression of Ash1l significantly increased fetal oocyte apoptosis.
- Reduced primordial follicle pool capacity was observed following Ash1l overexpression.
- Ash1l overexpression impaired DNA double-strand break repair and upregulated p63 and p-CHK2.
Conclusions:
- ASH1L acts as a crucial epigenetic regulator and genome guardian in fetal oocytes.
- ASH1L protects oocyte genome integrity by managing DNA damage response pathways.
- Dysregulation of ASH1L impacts oocyte quality and potentially female fertility.
Related Concept Videos
02:37DNA Damage can Stall the Cell Cycle
9.3K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.3K
01:30Apoptosis
11.8K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.8K
01:31The Intrinsic Apoptotic Pathway
6.7K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.7K
01:17The Extrinsic Apoptotic Pathway
6.5K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.5K
02:37DNA Damage Can Stall the Cell Cycle
2.7K
2.7K
02:25Overview of DNA Repair
31.4K
In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Chemically...
31.4K