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Chromosomal reciprocal translocation of the 4th and 20th chromosome. In genetics, chromosome translocation is a phenomenon that results in unusual rearrangement of chromosomes. This includes balanced and unbalanced translocation, with two main types: reciprocal, and Robertsonian translocation.
The symbol BCR is derived from breakpoint cluster region, a gene which encodes a protein that acts as a guanine nucleotide exchange factor for Rho GTPase proteins. [7] Translocation results in an oncogenic BCR-ABL1 gene fusion that can be found on the shorter derivative chromosome 22. This gene encodes for a BCR-ABL1 fusion protein.
The first fusion gene [1] was described in cancer cells in the early 1980s. The finding was based on the discovery in 1960 by Peter Nowell and David Hungerford in Philadelphia of a small abnormal marker chromosome in patients with chronic myeloid leukemia—the first consistent chromosome abnormality detected in a human malignancy, later designated the Philadelphia chromosome. [3]
The bHLH motif allows Myc proteins to bind with DNA, while the leucine zipper TF-binding motif allows dimerization with Max, another bHLH transcription factor. Myc mRNA contains an IRES (internal ribosome entry site) that allows the RNA to be translated into protein when 5' cap -dependent translation is inhibited, such as during viral infection.
The balanced translocation figure shows a 14/21 translocation between the long arms of chromosomes 14 and 21, where the other chromosomes are not shown. The individual has two copies of everything on chromosome 14, and two copies of all of the material on the long arm of chromosome 21 (21q). The derivative chromosome 21, which contains only ...
It shows 22 homologous autosomal chromosome pairs, both the female (XX) and male (XY) versions of the two sex chromosomes, as well as the mitochondrial genome (at bottom left). In genetics, a chromosomal rearrangement is a mutation that is a type of chromosome abnormality involving a change in the structure of the native chromosome. [1]
Most fusions between EWS and FLI1 result from a t(11;22)(q24;q12) reciprocal chromosome translocation. [3] This translocation creates a chimeric transcript which fuses exons 1-7 of EWSR1 to exons 6-9 (or less commonly 5-9) of FLI1. [4] [5] It has recently been appreciated that almost half of EWS and FLI1 fusions are a result of chromoplexy. [6]
Balancer chromosomes were first used in the fruit fly by Hermann Muller, who pioneered the use of radiation for organismal mutagenesis. [2]In the modern usage of balancer chromosomes, random mutations are first induced by exposing living organisms with otherwise normal chromosomes to substances which cause DNA damage; in flies and nematodes, this usually occurs by feeding larvae ethyl ...