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The magical factor in frog eggs: How does MPF lead cells to enter the division stage?
Maturation-promoting factor, abbreviated as MPF, also known as mitosis promoting factor or M phase promoting factor, is a cyclin-Cdk complex that plays a key role in the cell cycle. As early as the 1970s, scientists discovered this promoting factor in frog oocytes. Studies have shown that during the cell cycle, MPF phosphorylates a variety of mitosis-related proteins, prompting cells to enter the M phase from the G2 phase, which is a process that is crucial for cell division.
Activation of MPF enables cells to undergo mitosis efficiently and ensures the correct transfer of genetic material.
Discovery of MPF
In 1971, two groups of researchers (Yoshio Masui and Clement Markert, and L. Dennis Smith and Robert Ecker) discovered that frog oocytes arrested in the G2 phase could be stimulated by microinjection of progesterone into oocytes. cytoplasm and enter the M phase. Since the process of oocyte entry into meiosis is often referred to as oocyte maturation, this cytoplasmic factor is called maturation-promoting factor (MPF). Further studies have shown that the activity of MPF is not limited to the meiosis of oocytes, but also exists in somatic cells, prompting them to enter the M phase of mitosis.MPF Structure
MPF is composed of two subunits: type III cyclin-dependent kinase 1 (CDK1) and cyclin.
CDK1 is a kinase subunit that is primarily responsible for phosphorylating specific serine and threonine residues of target proteins. Cyclin is a regulatory subunit that is essential for the function of the kinase subunit. These cyclins can be divided into type A and type B, and these cyclins have a nine-residue sequence called a "destruction box" in the N-terminal region, which enables them to be recognized and degraded by ubiquitin ligases. Degrade in time.
Role in the cell cycle
During the G1 and S phases, the CDK1 subgene is inactive due to an inhibitory enzyme called Wee1. Wee1 can phosphorylate the Tyr-15 residue of CDK1, making it inactive. During the transition from G2 phase to M phase, CDC25 dephosphorylates CDK1, enabling it to bind to cyclin B and promote the activation of MPF, thereby allowing cells to enter mitosis.
During the activation of MPF, the positive feedback mechanism further strengthens the signal for entering the M phase, effectively promoting the preparation of cells for division.
MPF Functional Overview
The main functions of MPF include promoting microtubule instability to trigger the formation of mitotic fibers, promoting chromosome condensation, and possibly phosphorylating nuclear fiber proteins in the nuclear membrane, ultimately leading to nuclear envelope depolymerization. In addition, MPF phosphorylates GM130, leading to fragmentation of the basal body and endoplasmic reticulum.MPF Targets
MPF affects numerous proteins involved in mitosis, including:
- Collectins promote the condensation of chromosomes.
- Various microtubule-associated proteins are involved in the formation of filaments.
- Nuclear fibronectin, promotes the degradation of the nuclear envelope.
- Histones H1 and H3.
- High matrix interstitial, leading to fragmentation.
Pseudo-vigilance regulation
MPF phosphorylates inhibitory sites on actin during early mitosis, which helps prevent cytokinesis from occurring. When MPF activity decreases during late divisions (e.g., the chromosome-free tract of anaphase), these inhibitory sites are dephosphorylated and cytokinesis is completed.
Anisohedral excision and negative feedback mechanism
Degradation of MPF is carried out during anaphase of mitosis by the heterodimer-promoting complex, which does so by polyubiquitination of cyclin B, marking it for protein degradation. This process results in a decrease in the concentration of the cyclin B/CDK1 complex after the end of mitosis, thereby ending the activity of MPF.
MPF not only plays a key role in the cell cycle, but its research reveals how cells divide under fine regulation to maintain the continuation of life. As science develops further, will we be able to find new ways to treat diseases from these cell cycle laws?
