Zaidman Lab

Principal Investigator

Nathan Zaidman, PhD

Assistant Professor, Biochemistry & Molecular Biology

Dr. Zaidman received his PhD in 2016 from the University of Minnesota under the mentorship of Scott M. O'Grady. He completed his postdoctoral fellowship with Jennifer Pluznick at Johns Hopkins University in 2022. He joined UNM Faculty in January 2023.

Interests

• Adhesion G protein-coupled receptors
• Renal physiology
• Acid-base homeostasis
• Epithelial cell physiology

Techniques

• Whole animal physiology using transgenic mice
• Immunofluorescent microscopy (confocal, spinning disc, high throughput)
• Calcium imaging, pH imaging
• RNAscope hybridization
• Tubule isolation from mouse kidney (microdissection)
• Flow cytometry and primary cell isolation
• Biochemistry assays (western blot, qPCR, immunoprecipitation)
• Molecular cloning

Current Members

Krystin Eaton, BS – Research Technician

Hailey Steichen, MS – Research Scientist

Jianxiang Xue, PhD – Postdoctoral Fellow

Teagan Yan, BS – Research Assistant

Former Members

Sophia Slora – Summer UPN Scholar (2023)

Research Projects

The overarching goal of the Zaidman lab is to determine the physiological significance of adhesion-class G protein-coupled receptors (aGPCRs). aGPCRs are unique signaling proteins that are self-activated by tethered-peptide agonists. These receptors convey extracellular forces into intracellular chemical signals. However, many aGPCRs have undefined roles. Our current efforts are focused on illuminating the functional roles of aGPCRs Gpr116, Gpr56 and Gpr126 in the kidney.

1. Gpr116 is a regulator of renal acid secretion.

Gpr116 (Adgrf5) localizes to A-type intercalated cells in the collecting ducts. Previous research revealed (PMID: 33004624) that genetic deletion of Gpr116 in mouse kidneys caused a significant reduction in urine pH due to physiologically inappropriate distribution of V-ATPase proton pumps on the surface of A-type cells. Our research goals are to identify the signaling pathway(s) downstream of Gpr116 that regulate V-ATPase surface expression in A-type intercalated cells, and to discover the endogenous activator of Gpr116 in the collecting duct.

• Eaton
• Steichen

2. Investigating the physiological significance of aGPCRs in the kidney.

Single-cell RNAseq experiments have revealed the expression pattern of several aGPCRs expressed throughout the kidney. Our goal is to determine the physiological significance of these receptors to better understand how the kidney maintains whole-body homeostasis and to develop novel therapeutic approaches to human disease.

• Xue

3. Characterization of the Foxi1-dependent transcriptome.

Foxi1 is a master regulator of V-ATPase proton pumps, as numerous studies have demonstrated its essential role in the development of specialized acid-secreting cells in the inner ear, epididymis, lungs, and kidney. FOXI1 transcriptionally activates several V-ATPase subunits, including Atp6v1b1 and Atp6v0a4, that uniquely localize the proton pump to the plasma membrane. Indeed, mice lacking Foxi1 develop distal renal tubular acidosis due to the loss of these essential V-ATPase subunits in intercalated cells. In fact, intercalated cells are entirely absent in Foxi1 null animals. Mutations to Foxi1 are also associated with Pendred syndrome, one of the most frequent forms of syndromic genetic deafness. While the physiological and pathological significance of Foxi1 has been firmly established, the complete transcriptional targets of Foxi1 have not. We recently demonstrated (PMID: 36603001) that overexpression of Foxi1 in an immortalized murine collecting duct cell line causes upregulation of several target genes. Our goal is to define the complete Foxi1-dependent transcriptome using this in vitro heterologous expression system.

• Slora
• Yan

Research Opportunities

If you are interested in performing research with our group, please contact Dr. Zaidman directly.

• Undergraduate research/honors thesis
• Prospective PhD students
• Postdoctoral fellowships

Major Funding

NIH/NIDDK R00DK127215 (Zaidman)

“Gpr116 Regulation of Renal Acid Excretion”