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Published on: February 16, 2015

Lovastatin triggers an apoptosis-like cell death process in the fungus Mucor racemosus

L V Roze1, J E Linz

  • 1Department of Food Science and Human Nutrition, Michigan State University, East Lansing 48824, USA.

Fungal Genetics and Biology : FG & B
|February 12, 1999
PubMed

Insights

Lovastatin induces apoptosis-like cell death in Mucor racemosus by affecting ras gene expression and protein processing. Cyclic adenosine monophosphate (cAMP) signaling pathways are crucial for regulating this developmental stage-specific cell death.

Area of Science:

  • Mycology
  • Cell Biology
  • Biochemistry

Background:

  • Mucor racemosus is a filamentous fungus exhibiting dimorphism.
  • Ras genes (Mras1, Mras2, Mras3) are implicated in fungal morphogenesis.
  • Lovastatin is an inhibitor of protein prenylation.

Purpose of the Study:

  • To investigate the effects of lovastatin on Mucor racemosus.
  • To characterize lovastatin-induced cell death.
  • To explore the role of cAMP in lovastatin-induced cell death.

Main Methods:

  • Treatment of Mucor racemosus with lovastatin.
  • Analysis of ras gene expression and protein processing.
  • Assessment of cell viability, morphology, and DNA fragmentation.
  • Investigation of the effects of dibutyryl-cAMP and wortmannin.

Main Results:

  • Lovastatin altered MRas1 processing, blocked MRas3 accumulation, and disrupted the MRas1/p20 complex.
  • Lovastatin induced apoptosis-like cell death, characterized by arrested germination, reduced growth, cell shrinkage, and DNA fragmentation.
  • Dibutyryl-cAMP prevented lovastatin-induced cell death, with a synergistic effect observed with wortmannin.

Conclusions:

  • Lovastatin induces an apoptosis-like cell death process in Mucor racemosus.
  • The observed cell death is dependent on ras gene expression and protein processing.
  • Signal transduction pathways involving cAMP are critical for regulating lovastatin-induced cell death during specific developmental stages.

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