Cait S. Kirby, PhD

I am the Associate Director of the Williams College Rice Center for Teaching.
I am a biologist with an interest in genetics, especially mitochondrial DNA and sex chromosomes.
I am an academic developer, learner, and teacher with interests in STEM identity, belonging, metacognition, and disability.
I promote inclusion in STEM and higher ed by facilitating belonging and creating accessible education resources.

PUBLICATIONS

Helms, Kirby, and Merrill 2022

Black text on a white background: Designing for Fatigue. Nic Helms, Cait Kirby, Asia Merrill, 27 January 2022, Design. Colorphoto of beige wodden pieces stacked on top of eahother precipitously per the children's game.
Below is the opening paragraph of the article: We’re currently living and working through the third year of a global pandemic, and the cumulative burden of fatigue weighs down our lives and our semesters.
As Beth McMurtie wrote in the Chronicle in 2020, “professors across the country are treading water, feeling overwhelmed and under-supported.”
We’ve known for a while that we should plan for fatigue during this global pandemic. Students, teachers, and disability justice activists have been prophesying the dangers of fatigue all along.
In particular, Aimi Hamraie has been beating the drum about opposing capitalist norms of productivity and slowing down teaching.
Here at Plymouth State University, the Intersectionality Talks with Helen Rottier and Justin Shaw have each addressed the need for less overwork and more care in our classrooms.

Here we discussed the challenges of teaching during the ongoing COVID-19 pandemic, as well as supportive teaching strategies.

Kirby and Fedesco 2020

Here we designed an activity for instructors of all levels to help identify and mitigate implicit biases.
Kirby 2020

Here I designed an online teaching strategy to promote belonging in the classroom and uplift quiet voices.

Kirby and Patel 2021

Black text on white background Elevated mitochondrial DNA copy number found in ubiquinone-deficient clk-1 mutants is not rescued by ubiquinone precursor 2-4-dihydroxybenzoate
Cait S Kirby 1, Maulik R Patel 2
Affiliations expand
PMID: 33581333 DOI: 10.1016/j.mito.2021.02.001
Abstract
Inside mitochondria reside semi-autonomous genomes, called mtDNA. mtDNA is multi-copy per cell and mtDNA copy number can vary from hundreds to thousands of copies per cell. The variability of mtDNA copy number between tissues, combined with the lack of variability of copy number within a tissue, suggest a homeostatic copy number regulation mechanism. Mutations in the gene encoding the Caenorhabditis elegans hydroxylase, CLK-1, result in elevated mtDNA. CLK-1's canonical role in ubiquinone biosynthesis results in clk-1 mutants lacking ubiquinone. Importantly, clk-1 mutants also exhibit slowed biological timing phenotypes (pharyngeal pumping, defecation, development) and an activated stress response (UPRmt). These biological timing and stress phenotypes have been attributed to ubiquinone deficiency; however, it is unknown whether the mtDNA phenotype is also due to ubiquinone deficiency. To test this, in animals carrying the uncharacterized clk-1 (ok1247) mutant allele, we supplemented with an exogenous ubiquinone precursor 2-4-dihydroxybenzoate (DHB), which has previously been shown to restore ubiquinone biosynthesis. We measured phenotypes as a function of DHB across a log-scale range. Unlike the biological timing and stress phenotypes, the elevated mtDNA phenotype was not rescued. Since CLK-1's canonical role is in ubiquinone biosynthesis and DHB does not rescue mtDNA copy number, we infer CLK-1 has an additional function in homeostatic mtDNA copy number regulation.

Keywords: 2-4-Dihydroxybenzoate; CLK-1; COQ-7; Copy number; Mitochondrial DNA; Ubiquinone.

Copyright © 2019 Elsevier B.V. and Mitochondria Research Society. All rights reserved. All rights reserved.

Here we tested whether elevated mtDNA copy number found in clk-1 mutants is due to loss of ubiquinone. We found that ubiquinone supplementation did not restore mtDNA copy number to wild type levels. Thus, we infer that the elevated copy number phenotype in clk-1 mutants is due to an additional role for CLK-1.

Gitschlag, et al 2016

Here we demonstrated the C. elegans mtDNA mutation uaDf5 escapes copy number regulation. This selfish genetic element (uaDf5) exploits the mitochondrial unfolded protein response to avoid mitophagy.
Kirby, et al 2016

Here we designed a teaching laboratory exercise for young scientists to learn about their own DNA. Students extract their DNA and genotype themselves for an inversion polymorphism on the long arm of the X chromosome.