Sarah Van Oeveren ACF Abstract FY12

Characterization of PkndlnΔ5, a derivative allele of the delorean mutation associated with the Protein kinase N gene in Drosophila melanogaster.

53rd Annual Drosophila Research Conference

The delorean mutation in Drosophila melanogaster was identified from a collection of mutants generated in a large-scale screen of P[IacW] transposon insertions on the second chromosome (Torok et al 1993 Genetics 135: 71-80). Wings of flies that are homozygous for the delorean mutation are held away from the body, noticeably curved downward and have additional defects of the wing margin. The P[IacW] insertion has been mapped to the first intron of the Drosophila Protein kinase N gene (Pkn) and the delorean mutation is thought to alter Pkn function (Ostrow and Momin 2001 A. Dros. Res. Conf. 42: 701B). The delorean wing phenotype is only seen when the P[IacW] insertion is homozygous (i.e Pkndln/ Pkndln), yet is not due to a loss-of-function mutation as evidenced by the wild-type phenotype observed when Pkndln is heterozygous with a deficiency (Df(2R)45C) that removes the Pkn gene. This is in contrast to other Pkn alleles such as Pkn06736; a null allele that results in dorsal closure defects during embryogenesis (Lu and Settleman 1999 Genes Dev. 13: 1168-1180). To understand the molecular basis of the delorean phenotype we have generated deletion derivatives of the Pkndln allele. One of these derivatives, Pkndln5, generates a less severe wing phenotype, but was found to have a profound effect on female fertility. In addition, Pkndln5 demonstrates that the delorean phenotype is transvection-dependent. We determined that the molecular lesion associated with the Pkndln5 allele was internal to the P[lacW] transposon, removing sequence from the mini-white+ gene. We present our continued analysis of the Pkndln5 derivative with respect to the role of the Pkn gene in wing morphogenesis as well as its prospective role in oogenesis.

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