All articles tagged with #cell division
Researchers built a three‑dimensional computer model that simulates nearly every chemical reaction in a minimal bacterial cell (JCVI‑Syn3a), producing a virtual cell that copies its DNA and divides in about 105 minutes. The full simulation ran for six days on a supercomputer and required simplifying assumptions, but it demonstrated coherent, life‑like cellular processes across the cell cycle.
Researchers studying zebrafish embryos found that very large embryonic cells can divide without a fully closed actin contractile ring. Instead, they use a 'mechanical ratchet' system where cytoskeletal fibers and cycles of cytoplasmic stiffness—stabilized by microtubules—drive the contractile band inward step by step across several cell cycles, reshaping textbook views of cytokinesis in large eggs.
Researchers from the Brugués group at TU Dresden report in Nature a new mechanism for early embryonic cell division in yolk-rich cells: a mechanical ratchet that drives division without a fully closed actin contractile ring. By showing microtubule asters stiffen the cytoplasm during interphase and the cytoplasm becomes more fluid in M-phase, they find the actin band can ingress across multiple cell cycles, anchored by microtubules and re-stabilized when the cytoplasm stiffens again. This challenges textbook models and may apply broadly to yolk-rich embryos across species.
Researchers at the Ruđer Bošković Institute have discovered that the protein CENP-E's primary role in cell division is to stabilize initial chromosome attachments rather than act as a motor protein, overturning two decades of textbook understanding and highlighting new implications for cancer and genetic disease research.
A recent study uncovers how the 'jumping gene' LINE-1 hijacks cell division processes by forming condensates with proteins to enter the nucleus and copy itself, providing insights into genome evolution and potential therapeutic targets.
Scientists have discovered a "mitotic stopwatch" mechanism that allows individual cells to remember and respond to problems during cell division. This system involves a complex of proteins, including p53, which forms when mitosis takes longer than usual. The complex, consisting of p53, ubiquitin-specific protease 28, and p53-binding protein 1, helps stabilize p53 and can stop future cell divisions if present at high levels. Defects in this mechanism are frequently found in tumor samples, highlighting its role in tumor suppression. This discovery sheds light on how cells store memories of cell division problems and adds to the complex network of pathways involving p53 in cellular activities.
Scientists in Spain have captured the first detailed images of a human cell's microtubule formation process, shedding light on how these structures are built during cell division. The discovery could lead to targeted treatments for cancer and other conditions, as microtubules play a crucial role in cell biology. The high-resolution visuals and atomic-scale film reveal the intricate process of microtubule nucleation and the role of the gamma-tubulin ring complex (γ-TuRC) in guiding their formation. Understanding this process may offer new therapeutic approaches and insights into preventing cancer cells from dividing.
Researchers have captured the first atomic-scale "movie" showing how human cells initiate the construction of microtubules, crucial structures involved in cell division and various cellular functions. The study, published in Science, reveals the process of microtubule nucleation, shedding light on the formation of these tiny tube-shaped structures and their role in pulling apart duplicated genetic material during cell division. The findings provide fundamental insights with potential implications for treating diseases such as cancer and neurodevelopmental disorders, offering a basis for developing more targeted therapeutic approaches.
New research challenges the traditional understanding of how microtubule poisons, a class of cancer drugs, work. Instead of simply halting cancer cell division, these drugs alter the process, sometimes causing new cancer cells to die. The study sheds light on why previous attempts to discover new chemotherapy drugs based on stopping cell division have been disappointing. Researchers now suggest focusing on disrupting the cell division process differently to improve cancer treatments.
Researchers have discovered that the midbody remnant, previously thought to be a cellular waste product, contains genetic material that can influence the fate of other cells, including promoting the development of cancer. The midbody, formed during cell division, contains RNA and cellular machinery necessary for protein production. These RNA blueprints are not related to cell division but instead play a role in cell communication and activities such as pluripotency and oncogenesis. Midbody remnants can be released into the bloodstream and taken up by other cells, potentially altering their behavior. The findings suggest that targeting midbody RNA could be a promising approach for cancer detection and therapeutics.
Researchers have developed a new imaging process called PINE nanoscopy, which uses scattered light instead of fluorescent molecules to observe cellular processes like cell division. By imaging randomly distributed gold nanorods, the system allows for longer observations at a highly detailed resolution. Using this technique, scientists were able to observe the behavior of actin molecules during cell division, discovering that actin expands when the cell contracts and vice versa. This breakthrough could lead to a better understanding of how molecular defects in tissues and organs contribute to disease development.
A study conducted by biophysicists from the University of Chicago has found that living cells in confinement behave similarly to people in crowds. The researchers observed that cells adjust their size while growing alongside other cells in sheets of tissue. The study provides insights into how cells regulate their growth and division, which is crucial for understanding tissue development and growth. The findings may have implications for cancer treatments and tissue engineering.
Researchers led by Martin Thanbichler have discovered a central regulator, DipM, that controls different classes of autolysins involved in bacterial cell wall remodeling. DipM interacts with multiple autolysins and a cell division factor, making it the first identified regulator that can control two classes of autolysins. Disruption of DipM leads to cell death, highlighting its critical role in cell shape maintenance and division. These findings may contribute to the development of new therapeutic strategies against bacterial infections by targeting multiple autolytic pathways simultaneously.
Scientists have discovered that certain long-lived fungi species can use a special type of cell division called a "clamp connection" to prevent the accumulation of damaging mutations, similar to cancers in humans and plants. This mechanism allows the fungi to live longer by avoiding the development of harmful mutations. The fungi's nuclei continuously test each other for the ability to fuse, and mutations in fusion genes fail this test, leading to a dead-end for the cell. This finding adds to the understanding of how organisms evolve mechanisms to avoid cancerous mutations and live longer lives.
Researchers at Wageningen University have discovered that long-lived fungi have evolved a mechanism to prevent the accumulation of life-limiting mutations. These fungi use a special type of cell division called a 'clamp connection' to screen against selfish mutants, allowing them to live for centuries without accumulating too many genetic faults. This finding sheds light on the biological tension between individual cells and whole organisms, similar to cancer in other organisms. While the study may not directly translate to cancer prevention in humans, it highlights the various ways evolution equips organisms to overcome challenges and maintain longevity.