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Updated: Jun 28, 2025

Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
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Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis

Published on: March 19, 2019

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Mitochondria complex I deficiency in Candida albicans arrests the cell cycle at S phase through suppressive TOR and

Lulu Zhang1,2, Zhou Meng3, Richard Calderone2

  • 1Department of Dermatology, Jiangsu Province Hospital of Traditional Chinese Medicine, No.155 Hanzhong Road, Qinhuai District, Nanjing, 210029, China.

FEMS Yeast Research
|April 9, 2024
PubMed

Insights

Mitochondrial electron transport chain (ETC) mutations disrupt the cell cycle in Candida albicans. This study reveals how ETC complex mutations impact cell cycle progression and longevity through key signaling pathways.

Area of Science:

  • * Molecular biology
  • * Cellular biology
  • * Mycology

Background:

  • * The mitochondrial electron transport chain (ETC) is crucial for cellular respiration and energy production.
  • * The cell cycle is a tightly regulated process essential for cell growth and division.
  • * Candida albicans, an opportunistic fungal pathogen, relies on mitochondrial function for virulence and survival.

Purpose of the Study:

  • * To investigate the impact of mutations in mitochondrial ETC complexes (CI, CIII, CIV) on the cell cycle progression of Candida albicans.
  • * To elucidate the roles of specific ETC components in regulating cell cycle dynamics and cellular processes.
  • * To explore the relationship between ETC function, cell cycle control, and key signaling pathways (cAMP/PKA, TOR1, Snf1).

Main Methods:

  • * Generation of genetic null mutants for ETC complexes I (CI), III (CIII), and IV (CIV) in Candida albicans.
  • * Analysis of cell cycle stages (G0/G1, S, G2/M) using fluorescence-activated cell sorting (FACS).
  • * Measurement of cell size and assessment of gene transcription (e.g., RIM15).

Main Results:

  • * CI null mutants showed altered cell cycle progression, including extended S phase and reduced G2/M populations.
  • * CIII mutants exhibited an increased G1/G0 phase population.
  • * Specific CI mutants (ndh51Δ/Δ, goa1Δ/Δ) displayed cell cycle aberrations linked to cAMP/PKA downregulation, while others (nuo1Δ/Δ, nuo2Δ/Δ) showed increased RIM15 transcription.

Conclusions:

  • * Mutations in mitochondrial ETC proteins significantly disrupt the cell cycle in Candida albicans.
  • * The interplay between ETC function, cell cycle progression, and signaling pathways (cAMP/PKA, TOR1, Snf1) is critical for fungal growth and longevity.
  • * Understanding these mechanisms provides insights into fungal pathogenesis and potential therapeutic targets.
Keywords:
C. albicans mitochondrial CI subunit proteinsTOR signalingcAMP signalingcell cycle

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