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- Academic Editor
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Background: Bruton’s tyrosine kinase (BTK) is a non-receptor type
tyrosine kinase originally identified as the genetic signature responsible for
X-linked agammaglobulinemia (XLA) when mutated. Its functional form is required
for B lymphocyte maturation in both humans and mice, whereas loss-of-function
causes a different form of developmental defect in the fruit fly,
Drosophila melanogaster. Methods: Ibrutinib and other
therapeutic inhibitors of BTK have been extensively used to successfully treat
various leukemias and lymphomas. Btk29A type 2 is the ortholog of BTK in
the fruit fly. We show that feeding wild-type flies an ibrutinib-containing diet
induces phenocopying of Btk29A mutants, i.e., failure in the fusion of
left and right halves of the dorsal cuticles, partial loss of wing tissues and
dysregulation of germ cell production. Results: We have previously
reported that Btk29A phosphorylates Drosophila Arm (