A mechanistic view on the evolutionary origin for centrin-based control of centriole duplication.
Mounting evidence implicates the protein centrin as a key regulator of centriole duplication, yet it remains to be determined just how centrin functions in this process. Recent studies suggest that centrin exerts both spatial and temporal control over centriole duplication through its role as a component of centriole precursor structures and through periodic cell-cycle specific changes in its abundance. Here, an overview of centrin and its role in centrosome dynamics is presented. Finally, a speculative model for just how centrin may operate to control centriole duplication is proposed with the intention to stimulate future advances in this area. This model provides an evolutionary basis for the preservation of essential features of the yeast spindle pole body (SPB) with the origin of the complex structure of the mammalian centriole.
Salisbury
Jeffrey L
JL
Department of Biochemistry and Molecular Biology, Tumor Biology Program, Mayo Clinic, Rochester, Minnesota, USA. salisbury@mayo.edu
D000818:Animals; D005075:Biological Evolution; D002135:Calcium-Binding Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D002453:Cell Cycle / Q000502:physiology; D018797:Cell Cycle Proteins / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D002502:Centrioles / Q000378:metabolism* / Q000648:ultrastructure; D018385:Centrosome / Q000378:metabolism / Q000648:ultrastructure; D006801:Humans; D008958:Models, Molecular; D010766:Phosphorylation; D017434:Protein Structure, Tertiary
C472752:CETN2 protein, human; D002135:Calcium-Binding Proteins; D018797:Cell Cycle Proteins