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Role of type I myosins in receptor-mediated endocytosis in yeast
1Department of Biochemistry, Biozentrum, University of Basel, Klingelbergstrasse 70, Basel, Switzerland.
Abstract:
Type I myosins are thought to drive actin-dependent membrane motility, but the direct demonstration in vivo of their involvement in specific cellular processes has been difficult. Deletion of the genes MYO3 and MYO5, which encode the yeast type I myosins, almost abolished growth. A double-deleted mutant complemented with a MYO5 temperature-sensitive allele (myo5-1) showed a strong defect in the internalization step of receptor-mediated endocytosis, whereas the secretory pathway remained apparently unaffected. Thus, myosin I activity is required for a budding event in endocytosis but not for several other aspects of membrane traffic.
Insights
Yeast type I myosins (MYO3 and MYO5) are crucial for cell growth. Deleting these genes severely impairs receptor-mediated endocytosis, specifically the internalization step, highlighting their essential role in this cellular process.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Type I myosins are implicated in actin-dependent membrane dynamics.
- In vivo evidence for their specific roles in cellular processes has been limited.
Purpose of the Study:
- To investigate the in vivo function of yeast type I myosins (encoded by MYO3 and MYO5).
- To determine the specific cellular processes dependent on type I myosin activity.
Main Methods:
- Gene deletion of MYO3 and MYO5 in yeast.
- Complementation of a double deletion mutant with a temperature-sensitive MYO5 allele (myo5-1).
- Analysis of membrane traffic, including endocytosis and secretion.
Main Results:
- Deletion of MYO3 and MYO5 genes almost abolished yeast growth.
- The myo5-1 mutant exhibited a significant defect in the internalization step of receptor-mediated endocytosis.
- The secretory pathway appeared unaffected in the mutant.
Conclusions:
- Yeast type I myosin activity is essential for a budding event during endocytosis.
- Type I myosins are not required for all aspects of membrane traffic, such as secretion.