Publication Date:
1996-04-26
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geli, M I -- Riezman, H -- New York, N.Y. -- Science. 1996 Apr 26;272(5261):533-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Biozentrum, University of Basel, Klingelbergstrasse 70, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614799" target="_blank"〉PubMed〈/a〉
Keywords:
Alleles
;
Endocytosis/*physiology
;
Gene Deletion
;
Molecular Sequence Data
;
Mutation
;
Myosins/genetics/*physiology
;
Peptides/metabolism
;
Receptors, Mating Factor
;
Receptors, Peptide/metabolism
;
Saccharomyces cerevisiae/genetics/*physiology
;
Temperature
;
*Transcription Factors
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
