Rapamycin induces morphological and physiological changes without increase in lipid content in Ustilago maydis

Lucero Romero-Aguilar1, Guadalupe Guerra-Sánchez2, Eda P Tenorio1

  • 1Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, 04510, Mexico City, Mexico.

Archives of Microbiology
|February 24, 2020
PubMed

Insights

Rapamycin treatment of Ustilago maydis inhibits Target of Rapamycin Complex 1 (TORC1), affecting cell division and causing lipid bodies to fuse. This study reveals TORC1

Area of Science:

  • Mycology
  • Cell Biology
  • Biochemistry

Background:

  • The conserved serine/threonine kinase TOR forms TORC1, regulating key cellular processes like ribosome biogenesis, autophagy, and lipid metabolism.
  • TORC1 influences cell cycle progression, specifically extending the G2 phase.
  • Rapamycin is a known inhibitor of TORC1.

Purpose of the Study:

  • To investigate the impact of rapamycin on cell growth, morphology, and neutral lipid metabolism in the phytopathogenic fungus Ustilago maydis.
  • To elucidate the role of TORC1 in U. maydis cellular physiology.

Main Methods:

  • Treatment of U. maydis with rapamycin.
  • Microscopic analysis of cell morphology and lipid body formation.
  • Staining techniques (Blue-CMAC and BODIPY) for organelle differentiation.

Main Results:

  • Rapamycin-induced TORC1 inhibition led to septa formation, separating post-mitotic nuclei.
  • Accumulation of triacylglycerols was not observed, but large lipid bodies formed, suggesting fusion of smaller ones.
  • Vacuoles exhibited behavior similar to lipid bodies, yet double labeling confirmed their independence.

Conclusions:

  • TORC1 plays a significant role in regulating cell morphology in U. maydis.
  • TORC1 influences neutral lipid metabolism and the dynamics of lipid bodies.
  • TORC1 impacts vacuolar physiology and its relationship with lipid bodies in U. maydis.