Kyle Cunningham

About

Kyle Cunningham is a Professor in the Department of Biology at Johns Hopkins University. His research focuses on understanding the molecular mechanisms governing drug resistance and virulence in pathogenic yeasts, particularly Candida glabrata. Cunningham's laboratory has developed innovative approaches, such as adapting Tn-seq (transposon mutagenesis coupled to next-generation DNA sequencing), to perform genome-wide screens that identify genes mediating antifungal resistance, colonization, invasion, survival within immune cells, and virulence in hosts. His work aims to elucidate how C. glabrata acquired its pathogenic capabilities and resistance traits, which are significant given the increasing incidence of infections and resistance in clinical settings. Cunningham's background includes a PhD from UCLA, postdoctoral training in mitochondrial membrane biogenesis at the University of Basel, and yeast genetics at the Whitehead Institute at MIT. He rejoined Johns Hopkins as an assistant professor in 1994 and has since contributed extensively to the understanding of fungal pathogenesis and resistance mechanisms.

Research topics

• Biology
• Computational biology
• Genetics
• Biochemistry
• Botany
• Cell biology
• Microbiology

Selected publications

• Acidic calcium stores of Saccharomyces cerevisiae

  Cell Calcium · 2011-03-07 · 118 citations

  review1st authorCorresponding
  PublisherDOI

• A LAPF/phafin1-like protein regulates TORC1 and lysosomal membrane permeabilization in response to endoplasmic reticulum membrane stress

  Molecular Biology of the Cell · 2015-10-29 · 75 citations

  articleOpen accessSenior authorCorresponding

  Lysosomal membrane permeabilization (LMP) is a poorly understood regulator of programmed cell death that involves leakage of luminal lysosomal or vacuolar hydrolases into the cytoplasm. In Saccharomyces cerevisiae, LMP can be induced by antifungals and endoplasmic reticulum stressors when calcineurin also has been inactivated. A genome-wide screen revealed Pib2, a relative of LAPF/phafin1 that regulates LMP in mammals, as a pro-LMP protein in yeast. Pib2 associated with vacuolar and endosomal li…

  PublisherOA PDFDOI

• Vacuolar H+-ATPase (V-ATPase) Promotes Vacuolar Membrane Permeabilization and Nonapoptotic Death in Stressed Yeast

  Journal of Biological Chemistry · 2012-04-17 · 57 citations

  articleOpen accessSenior author

  Stress in the endoplasmic reticulum caused by tunicamycin, dithiothreitol, and azole-class antifungal drugs can induce nonapoptotic cell death in yeasts that can be blocked by the action of calcineurin (Cn), a Ca(2+)-dependent serine/threonine protein phosphatase. To identify additional factors that regulate nonapoptotic cell death in yeast, a collection of gene knock-out mutants was screened for mutants exhibiting altered survival rates. The screen revealed an endocytic protein (Ede1) that can…

  PublisherOA PDFDOI

• Identification of Essential Genes and Fluconazole Susceptibility Genes in <i>Candida glabrata</i> by Profiling <i>Hermes</i> Transposon Insertions

  G3 Genes Genomes Genetics · 2020 · 53 citations

  Senior authorCorresponding

  , which consume and generate alpha-ketoglutarate in mitochondria, exhibited increased and decreased resistance to fluconazole through a process that depended on Pdr1. These findings establish the utility of transposon insertion profiling in forward genetic investigations of this important pathogen of humans.

  PublisherOA PDFDOI

• Activation of an Essential Calcium Signaling Pathway in Saccharomyces cerevisiae by Kch1 and Kch2, Putative Low-Affinity Potassium Transporters

  Eukaryotic Cell · 2012-12-02 · 33 citations

  articleOpen accessSenior author

  In the budding yeast Saccharomyces cerevisiae, mating pheromones activate a high-affinity Ca(2+) influx system (HACS) that activates calcineurin and is essential for cell survival. Here we identify extracellular K(+) and a homologous pair of transmembrane proteins, Kch1 and Kch2 (Prm6), as necessary components of the HACS activation mechanism. Expression of Kch1 and especially Kch2 was strongly induced during the response to mating pheromones. When forcibly overexpressed, Kch1 and Kch2 localized…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21NS074072

  NIH · $158k · 2013

• NIH Grant R01GM053082

  NIH · $3.6M · 2009

• Functional genomics using auxin-inducible deletion analyses (AIDA)

  NIH · $434k · 2014–2018

Frequent coauthors

• Gerald R. Fink

  Whitehead Institute for Biomedical Research

  20 shared

• Zhengchang Su

  University of North Carolina at Charlotte

  16 shared

• Richard B. Marchase

  16 shared

• J. Edwin Blalock

  16 shared

• Feng Liang

  Wenzhou Medical University

  16 shared

• Jeffrey F. Harper

  University of Nevada, Reno

  16 shared

• Heven Sze

  University of Maryland, College Park

  16 shared

• Andrej Bugrim

  12 shared

Similar researchers at Johns Hopkins University

• Michael Schatzh-111
• Yumi Kimh-64
• Erik Andersenh-46