chimeric gene

The functions of many chimeric genes are not yet known.

Chimeric genes are important players in the evolution of genetic novelty.

Chimeric genes can form through several different means.

Nearby sequences were recruited to form an intron and an exon of this chimeric gene.

Finally, ectopic recombination, when there is an exchange between portions of the genome that are not actually related, can also produce chimeric genes.

Chimeric genes form through the combination of portions of one or more coding sequences to produce new genes.

One of the most well known chimeric genes was identified in Drosophila and has been named Jingwei.

The tobacco was infected with Agrobacterium transformed with this plasmid resulting in the chimeric gene being inserted into the plant.

Depending on where the new retrogene appears, it can recruit new exons to produce a chimeric gene.

For example the functional, chimeric gene 'jingwei' in 'Drosophila' was once thought to be a processed pseudogene.

Less frequently, longer-range productive recombinations through HLA genes have been noted producing chimeric genes.

Not listed here are the many kinds of cancers involving aberrant transcriptional regulation owing to creation of chimeric genes through pathological chromosomal translocation.

Chimeric genes can also form through retrotransposition where a retrotransposon accidentally copies the transcript of a gene and inserts it into the genome in a new location.

In addition, four out of five of these patients had detectable somatic RET/PTC chimeric genes.

Many chimeric genes form through errors in DNA replication or DNA repair so that pieces of two different genes are inadvertently combined.

It is a chimeric gene, originating from a retroposed sequence of the ATP synthase chain F gene from chromosome 2 to chromosome 4.

It was developed by Michael Bevan, Richard B. Flavell and Mary-Dell Chilton by creating a chimeric gene that joined an antibiotic resistant gene to the T1 plasmid from Agrobacterium.

Further studies are needed to show whether other genetic factors such as the RET/PTC chimeric gene are independently responsible for or cooperative with APC mutations in causing papillary thyroid cancers in FAP patients.