Answer:
The answer is reciprocal chromosomal translocation
Explanation:
The Philadelphia chromosome (Ph) is the truncated chromosome 22 generated by the reciprocal translocation t(9;22)(q34;q11) and was first identified in 1960 in a patient with CML [3]. Translocation of the proto-oncogene tyrosine-protein kinase (ABL1) gene located on chromosome 9 to the breakpoint cluster region (BCR) gene located on chromosome 22 results in a BCR-ABL1 fusion gene on the Ph [4, 5]. Three BCR-ABL1 fusion gene hybrids encode BCR-ABL1 protein isoforms p210, p190, and p230, which have persistently enhanced tyrosine kinase (TK) activity. These aberrantly activated kinases disturb downstream signaling pathways, causing enhanced proliferation, differentiation arrest, and resistance to cell death [6, 7]. Tyrosine kinase inhibitors (TKIs) targeting the BCR-ABL1 protein are the most successful targeted therapy for Ph-positive leukemia.
They all need to maintain homoestasis on land.
Answer:
C. They all use a cut and paste mechanism.
Explanation:
DNA transposons can go through a replicative or nonreplicative transposition.
The replicative transposition uses a "copy and paste" mechanism that consists of the introduction of a new copy of the transposable element in a new position, meanwhile <u>the old copy remains in the original position</u>. This determines an increase in the number of copies.
The nonreplicative transposition uses a "cut and paste" mechanism that consists of the cleavage of the transposable element from its position and its <u>insertion in a new position</u> without increasing the number of copies.
Retrotransposons, on the other side, move through RNA intermediates generated by the reverse transcriptase.
