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Non-homologous end joining can also join two different chromosomes together that had broken ends. The reason non-reciprocal translocations are dangerous is the possibility of producing a dicentric chromosome – a chromosome with two centromeres. When dicentric chromosomes form, a series of events can occur called a breakage-fusion-bridge cycle ...
Copy number variation was initially thought to occupy an extremely small and negligible portion of the genome through cytogenetic observations. [12] Copy number variations were generally associated only with small tandem repeats or specific genetic disorders, [13] therefore, copy number variations were initially only examined in terms of specific loci.
Duplications arise from an event termed unequal crossing-over that occurs during meiosis between misaligned homologous chromosomes. The chance of it happening is a function of the degree of sharing of repetitive elements between two chromosomes. The products of this recombination are a duplication at the site of the exchange and a reciprocal ...
The ability for mammals to tolerate aneuploidies in the sex chromosomes arises from the ability to inactivate them, which is required in normal females to compensate for having two copies of the chromosome. Not all genes on the X chromosome are inactivated, which is why there is a phenotypic effect seen in individuals with extra X chromosomes.
Replication is initiated at multiple origins of replication on multiple chromosomes simultaneously so that the duration of S phase is not limited by the total amount of DNA. [1] This flexibility in genome size comes at a cost: there has to be a high-fidelity control system that coordinates multiple replication origins so that they are activated ...
In UPD, a person receives two copies of a chromosome, or part of a chromosome, from one parent and no copies from the other parent due to errors in meiosis I or meiosis II. This acquired homozygosity could lead to development of cancer if the individual inherited a non-functional allele of a tumor suppressor gene.
We also know that the replication-timing program changes during development, along with changes in the expression of genes. For many decades now, it has been known that replication timing is correlated with the structure of chromosomes. For example, female mammals have two X chromosomes. One of these is genetically active, while the other is ...
As the cell divides, the telomeres on the ends of chromosomes shorten. The Hayflick limit is the limit on cell replication imposed by the shortening of telomeres with each division. This end stage is known as cellular senescence. The Hayflick limit has been found to correlate with the length of the telomeric region at the end of chromosomes.