Determination Of The Essential Functions Of A Conserved Cyclin, Cyclin Y, In Drosophila

<p>The Drosophila gene <i>CG14939</i> encodes a member of a highly conserved family of cyclins, the Y type cyclins, which have not been functionally characterized in any organism. Here I report the generation and phenotypic characterization of a null mutant of <i>CG14939</i>, which we rename <i>Cyclin Y</i> (<i>CycY</i>). I show that the null mutant, <i>CycY^E8</i>, is homozygous lethal with most mutant animals arresting during pupal development. The mutant exhibits delayed larval growth and major developmental defects during metamorphosis. Heat shock-induced expression of <i>CycY</i> at different times during development resulted in variable levels of rescue, the timing of which suggests a key function for zygotic <i>CycY</i> during the transition from third instar larvae to prepupae. <i>CycY</i> also plays an essential role during embryogenesis since zygotic null embryos from null mothers fail to hatch into first instar larvae. Furthermore I show that <i>CycY</i> is required for adult viability, especially in males. I provide evidence that the <i>CycY</i> protein (CycY) interacts with Eip63E, a Cyclin-dependent kinase (Cdk) for which no cyclin partner had previously been identified. Like <i>CycY</i>, the <i>Eip63E</i> gene has essential functions during embryogenesis, larval development, and metamorphosis. My data suggest that CycY/Eip63E form a cyclin/Cdk complex that is essential for several developmental processes.</p> <p> To gain insight into the cellular functions of CycY and to identify signaling pathways to which it belongs, I used RNA interference (RNAi) to knock down <i>CycY</i> expression in specific tissues. I show that <i>CycY</i> is required for wing growth and wing vein development. I also show that <i>CycY</i> genetically interacts with <i>Snr1</i> and <i>Brm</i>, two components of the Brm ATP-dependent chromatin remodeling complex, and that CycY can physically interact with Snr1. Furthermore, I show that downstream targets of the Brm complex are misregulated in <i>CycY</i> mutants. Taken together, these data suggest that <i>CycY</i> may be involved in gene regulation by modulating Brm complex activity.</p>

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Open Access Dissertation

Discipline thesis:degree_discipline

Molecular Biology and Genetics

Year dc:date.available

2010

Author dc:creator

• Liu, Dongmei

Contributors dc:contributor

• Russell L. Finley, Jr

• Brm
• Cdk14
• cyclin
• CycY
• Eip63E
• Snr1
• Genetics

Repository record dc:identifier

https://digitalcommons.wayne.edu/oa_dissertations/20

OAI identifier oai:identifier

oai:digitalcommons.wayne.edu:oa_dissertations-1019