Break-induced Replication
Break-induced Replication - Related Videos
11:19
Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System
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2016
We describe here a system utilizing a site-specific, reversible in vivo protein block to stall and collapse replication forks in Escherichia coli. The establishment of the replication block is evaluated by fluorescence microscopy and neutral-neutral 2-dimensional agarose gel electrophoresis is used to visualize replication intermediates.
02:40
DNA Replication
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2020
DNA replication involves the separation of the two strands of the double helix, with each strand serving as a template from which the new complementary strand is copied. After replication, each double-stranded DNA includes one parental or “old” strand and one “new” strand. This is known as semiconservative replication. The resulting DNA molecules have the same sequence and are divided equally into the two daughter cells. Replication in Prokaryotes DNA replication uses a large number of...
10:36
Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis
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Cited by 2 •
2010
We present a procedure by which two-dimensional agarose-gel analysis can be used to identify the structure of replication intermediates that occur following UV irradiation.
01:29
The “Break-Even” Point
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2025
The macroeconomic consumption function illustrates the relationship between aggregate consumption (C) and national income (Y). It is typically expressed as:C = a + bYwhere a denotes autonomous consumption—expenditures that occur regardless of income—and b, the marginal propensity to consume (MPC), indicates the fraction of additional income that is spent.The break-even point occurs where:C = YSolving for income yields the break-even level of national income:At this level, the entire output...
02:04
Fixing Double-strand Breaks
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2020
The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
FAQs
The critical intermediate is the displacement loop formed after a broken DNA end invades a homologous sequence. This pairing provides a template that can recruit replication machinery to the damaged chromosome. Because the invading end initiates synthesis without a matching second broken end, the pathway can restore chromosome continuity from a single-ended lesion.
Break-induced replication is especially suited to lesions produced when a replication fork collapses, leaving one usable DNA end rather than a conventional two-ended break. That structural distinction determines how repair proceeds: synthesis can continue extensively from the invading end, rather than simply restoring the original local DNA arrangement. The pathway therefore links replication restart with chromosome repair.
Template switching adds flexibility but also uncertainty to the repair process. During extensive synthesis, the nascent strand can move between related template sequences instead of copying only its initial homologous region. Such switching can alter which chromosome segments are incorporated, helping explain why repair by BIR may produce rearrangements or other changes in genome structure.
A conceptual BIR workflow follows four events: a single-ended break forms, the exposed end invades a homologous sequence, a displacement loop recruits replication machinery, and the nascent strand undergoes extensive synthesis. The key analytical focus is the transition from invasion to long-range copying, because that stage connects repair completion with potential genome alterations.
Analysis of BIR can reveal more than whether a chromosome was repaired. The pathway may be associated with mutation, loss of heterozygosity, copy-number changes, and rearrangements. These outcomes provide distinct readouts of how repair altered genetic information, allowing researchers to connect a repair event with broader patterns of genome instability.
In genetics, this pathway provides a framework for understanding how cells preserve chromosome continuity while still generating genomic damage or change. Its consequences are relevant to inherited disease and cancer biology because the same repair activity that allows recovery from chromosome damage can also change allele representation, dosage, or arrangement. BIR therefore connects DNA repair mechanisms to disease-associated genome instability.