Event Title

Rescue of a Gain-of-Function Mutation in Drosophila melanogaster Affecting Wing Morphogenesis

Presentation Type

Poster/Portfolio

Presenter Major(s)

Cell and Molecular Biology

Mentor Information

Georgette Sass

Department

Biology

Location

Henry Hall Atrium 64

Start Date

11-4-2012 9:00 AM

Keywords

Life Science

Abstract

The delorean mutation in Drosophila melanogaster was isolated from a collection of mutants generated in a large-scale screen of P[lacW] transposon insertions on the second chromosome. Wings of flies that are homozygous for the delorean mutation are held perpendicular to the body, misshapen, and have defects of the wing margin. The P[lacW] insertion has been mapped to the first intron of the Drosophila Protein kinase N gene and the delorean mutation is thought to alter PKN function. It is known that PKN protein is required in embryogenesis because loss-of-function mutations disrupt the process of dorsal closure. This defect can be rescued if normal PKN protein is supplied. This loss-of-function mutation is in contrast to the gain-of-function mutation seen in delorean that affects wing morphogenesis. We have analyzed transgenic flies that contain the pkn cDNA under the control of a heat-shock promoter to determine if providing PKN protein can also rescue the delorean phenotype.

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Apr 11th, 9:00 AM

Rescue of a Gain-of-Function Mutation in Drosophila melanogaster Affecting Wing Morphogenesis

Henry Hall Atrium 64

The delorean mutation in Drosophila melanogaster was isolated from a collection of mutants generated in a large-scale screen of P[lacW] transposon insertions on the second chromosome. Wings of flies that are homozygous for the delorean mutation are held perpendicular to the body, misshapen, and have defects of the wing margin. The P[lacW] insertion has been mapped to the first intron of the Drosophila Protein kinase N gene and the delorean mutation is thought to alter PKN function. It is known that PKN protein is required in embryogenesis because loss-of-function mutations disrupt the process of dorsal closure. This defect can be rescued if normal PKN protein is supplied. This loss-of-function mutation is in contrast to the gain-of-function mutation seen in delorean that affects wing morphogenesis. We have analyzed transgenic flies that contain the pkn cDNA under the control of a heat-shock promoter to determine if providing PKN protein can also rescue the delorean phenotype.