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<p><i>Cryptococcus neoformans</i> is a pathogen affecting predominantly immunocompromised individuals. Epigenetic regulation is pivotal for controlling <i>C. neoformans</i> virulence traits. Null mutants of histone deacetylase (HDAC) genes demonstrate reduced virulence. Here, we employed scanning (SEM) and transmission electron microscopy (TEM) to examine the ultrastructure of <i>C. neoformans HDA1</i> and <i>HOS2</i> null mutant strains<i>.</i> SEM revealed unipolar budding in the H99, <i>hda1</i>∆ and <i>hos2</i>∆ strains, whereas the <i>hda1∆hos2</i>∆ double mutant displayed evident multipolar budding. The <i>hos2</i>∆ strain exhibited defective capsule. TEM analysis showed a thicker cell wall for <i>hda1</i>∆ in comparison to H99, while the <i>hos2</i>∆ and <i>hda1∆hos2</i>∆ mutants displayed thinner cell walls. The <i>hos2</i>∆ and <i>hda1∆/hos2</i>∆ strains exhibited mitochondrial swelling. The <i>hda1∆hos2</i>∆ mutant also presented morphological features suggestive of cell degeneration. These findings highlight the critical role of HDACs in <i>C. neoformans</i> morphogenesis, which is essential to host cell-yeast interaction.</p>

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Ultrastructural Features of Cryptococcus neoformans Histone Deacetylases Null Mutant Strains

  • 期刊论文

  • 发表日期：

    2025年12月9日

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  • Daniel Oliveira da Mata,
  • Lucas da Costa Campos,
  • Martha Viviana Roa-Cordero,
  • Ariane Pandolfo Silveira,
  • Ingrid Gracielle Martins da Silva,
  • Victor Carlos Mello,
  • Luís Alexandre Muehlmann,
  • Bergmann Morais Ribeiro,
  • Sônia Nair Báo,
  • Marcio José Poças-Fonseca

摘要

Cryptococcus neoformans is a pathogen affecting predominantly immunocompromised individuals. Epigenetic regulation is pivotal for controlling C. neoformans virulence traits. Null mutants of histone deacetylase (HDAC) genes demonstrate reduced virulence. Here, we employed scanning (SEM) and transmission electron microscopy (TEM) to examine the ultrastructure of C. neoformans HDA1 and HOS2 null mutant strains. SEM revealed unipolar budding in the H99, hda1∆ and hos2∆ strains, whereas the hda1∆hos2∆ double mutant displayed evident multipolar budding. The hos2∆ strain exhibited defective capsule. TEM analysis showed a thicker cell wall for hda1∆ in comparison to H99, while the hos2∆ and hda1∆hos2∆ mutants displayed thinner cell walls. The hos2∆ and hda1∆/hos2∆ strains exhibited mitochondrial swelling. The hda1∆hos2∆ mutant also presented morphological features suggestive of cell degeneration. These findings highlight the critical role of HDACs in C. neoformans morphogenesis, which is essential to host cell-yeast interaction.