Department Chair

Daniel L. Potts, Ph.D.

Date of Award

5-2020

Access Control

Campus-Only Access

Degree Name

Biology, M.A.

Department

Biology Department

Advisor

I. Martha Skerrett, Ph.D.

Department Home page

https://biology.buffalostate.edu/bio

First Reader

I. Martha Skerrett, Ph.D.

Second Reader

Derek L. Beahm, Ph.D.

Third Reader

Gregory J. Wadsworth, Ph.D.

Abstract

Connexin30.3 is one of many gap junction proteins responsible for intercellular communication in skin. The importance of connexins in human epithelial tissue is emphasized by the many hereditary skin disorders resulting from their alteration. Cx30.3 is highly expressed in the granular layer of human skin and has overlapping expression patterns with Cx26, Cx32, Cx43, and Cx31. Mutations in Cx30.3 are linked to the skin disease Erythrokeratodermia variabilis et progressiva (EKV). The goal of this study was to further understand the function of Cx30.3 and its interaction with other skin connexins. After expressing Cx30.3 in Xenopus oocytes, the oocytes were paired, and the gap junctions were characterized using dual cell two-electrode voltage clamp. This is the first report of exogenous expression and characterization of human Cx30.3 although mouse Cx30.3 was previously expressed in oocytes and characterized in the homotypic configuration (Henneman et al, 1992). Cx30.3 expressed consistently and formed homotypic channels (hCx30.3/hCx30.3). Cx30.3 also formed heterotypic channels with other beta-type connexins expressed in skin. Homotypic gap junctions formed by Cx30.3 displayed weak sensitivity to voltage with a Gmin of 0.29 and a V1/2 of 70 mV. These values are close to those reported for mouseCx30.3 (V1/2 = 72 mV; Gmin = 0.23; Henneman et al., 1992). This research sets the stage for characterization of Cx30.3 mutations that cause disease and research aimed at assisting patients with rare skin disorders.

Available for download on Friday, October 30, 2020

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