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The Histoplasma capsulatum cdc2 gene is transcriptionally regulated during the morphologic transition

G Di Lallo1, S Gargano, B Maresca

  • 1International Institute of Genetics and Biophysics, CNR, Naples, Italy.

Gene
|March 11, 1994
PubMed

Insights

Researchers isolated and characterized the cdc2 gene in Histoplasma capsulatum to understand fungal dimorphism. This gene

Area of Science:

  • Molecular Biology
  • Mycology
  • Genetics

Background:

  • Dimorphic fungi, like Histoplasma capsulatum, exhibit reversible morphological transitions between mycelial and yeast forms.
  • Understanding the molecular control of these transitions is crucial for comprehending fungal pathogenesis and biology.
  • The cdc2 gene is a key regulator of the cell cycle in eukaryotes, including fungi.

Purpose of the Study:

  • To isolate and characterize the cdc2 gene from Histoplasma capsulatum.
  • To investigate the role of the H. capsulatum cdc2 gene in the dimorphic transition.
  • To analyze the transcriptional regulation of the cdc2 gene during morphological changes.

Main Methods:

  • Isolation and characterization of the cdc2 gene from Histoplasma capsulatum.
  • Analysis of gene structure, including exons and introns.
  • cDNA cloning and sequencing to determine the protein product.
  • Homology analysis with cdc2 genes from other fungal species.
  • Transcriptional analysis during mycelial-yeast transitions.

Main Results:

  • A cdc2 gene was successfully isolated and characterized from H. capsulatum.
  • The gene encodes a protein with high homology to other fungal cdc2 proteins, containing the conserved PSTAIRE sequence.
  • The H. capsulatum cdc2 gene is transcriptionally regulated, with higher activity observed in the yeast phase compared to the mycelial phase.

Conclusions:

  • The H. capsulatum cdc2 gene plays a role in regulating the dimorphic transition.
  • Transcriptional regulation of cdc2 is a key mechanism controlling the yeast-mycelium morphological switch.
  • This study provides insights into the molecular basis of fungal dimorphism in a pathogenic species.

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