Adaptation controls the 60 million-year stasis of the Drosophila spermtail protein beta 2 tubulin.

Adaptation controls the 60 million-year stasis of the Drosophila spermtail protein beta 2 tubulin.

Presenter(s)

Alexander James Kirkby

Comments

Presentation: 10:45 a.m.-12:00 p.m., Kennedy Union Ballroom

Description

Why do some features evolve while others do not? A fundamental component of Drosophila spermtail, the beta2 tubulin protein, has not evolved in sequence in 60 million years. Is the beta2 protein an ideal configuration maintained throughout the eons by natural selection? Or is beta2 the only configuration able to support the extreme length of the Drosophila spermtail axoneme? Previous tests in which chimeric versions of the beta2 protein were tested for their ability to support a spermtail found that even small changes in beta2 sequence render it non-functional, supporting the hypothesis that beta2 is the only configuration capable of making a spermtail. But it is possible that there are alternate forms capable of supporting function, and beta2 has won competitions over these for 60 million years. Here we test this hypothesis by replacing beta2 with the human spermtail-generating tubulin H. sapiens beta 3, and determine its ability to support a fly spermtail. Preliminary results indicate beta 3 can replace beta 2 function, indicating beta two’s stasis is due to winning competitions through its ability to template exceptionally long spermtails.

Publication Date

4-20-2022

Project Designation

Independent Research

Primary Advisor

Mark G. Nielsen

Primary Advisor's Department

Biology

Keywords

Stander Symposium project, College of Arts and Sciences

Adaptation controls the 60 million-year stasis of the Drosophila spermtail protein beta 2 tubulin.

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