What does BIR mean in BRITISH MEDICINE

Break-Induced Replication (BIR) is a process by which cells are able to repair double stranded breaks in DNA molecules. It is an alternative pathway of DNA replication to the more common semi-conservative mechanism, and it involves breaking the two strands of an existing molecule of DNA, using the broken strands as primers for building new strands of DNA, and then finally rejoining the newly formed molecules at the breakpoint.

Semi-conservative replication is a canonical replication pathway in which each strand of parental double-stranded DNA separates and serves as a template for newly synthesized complementary daughter strands. In contrast, BIR occurs when one or both of the parental strands become completely degraded but still remain linked at their 3’ ends and when these two 3’ ends act as primers for biosynthesis of new daughter strand(s).

BIR repairs all types of double strand breaks (DSBs), including those produced by chemicals, radiation, mechanical stress, and defects in base excision repair. In addition to these spontaneous damages, BIR can also be triggered artificially using restriction enzymes or exogenous agents such as gamma radiation or bleomycin.

BIR plays an important role in ensuring genetic stability because it enables cells to quickly and efficiently repair DSBs that occur due to various external factors. Without this process, cells would not be able to properly replicate their genome without error leading to accumulation of mutations with potentially harmful effects on cellular functions.

Yes, evidence suggests that mutations in genes related to homologous recombination (HR) repair pathways – including BIR – may be associated with some cancer syndromes and other diseases such as premature aging disorders like Werner Syndrome.

For some types of DSBs that occur within a gene sequence itself or close by it, yes – part or all of an intact sequence will serve as a template for synthesis during BIR. However, most frequently occurring DSBs don’t have a nearby template sequence available so they must rely on random nucleotide insertion instead.

Studies have suggested that humans employ both semi-conservative and break-induced replication mechanisms depending on the type and location of DSBs within our genomes. It has been found that certain human cell lines display higher levels of genomic instability when the pathways responsible for semi-conservative replication are inhibited while leaving those responsible for break-induced replication unimpaired - suggesting there may be some contribution from break induced repair even under physiological conditions.

While NHEJ relies solely on short sequences located next to each end being made compatible by ligation prior to resealing the break site; nonhomologous end joining does not require any preformed positive sequences within its vicinity nor does it involve any kind template sequencing either - making it better suited for closely located repetitive sites which could otherwise inhibit successful homology directed repair attempts via normal mechanisms.