Redundancy in the microfilament system: abnormal development of Dictyostelium cells lacking two F-actin cross-linking proteins.
We generated by gene disruption Dictyostelium cells that lacked both the F-actin cross-linking proteins, alpha-actinin and gelation factor. Several major cell functions, such as growth, chemotaxis, phagocytosis, and pinocytosis, were apparently unaltered. However, in all double mutants, development was greatly impaired. After formation of aggregates, cells were very rarely able to form fruiting bodies. This ability was rescued when mutant and wild-type strains were mixed in a ratio of 70 to 30. The developmental program in the mutant was not arrested, since the expression pattern of early and late genes remained unchanged. Development of the mutant was rendered normal when a functional alpha-actinin gene was introduced and expressed, showing the morphogenetic defect to be due to the absence of the two F-actin cross-linking proteins. These findings suggest the existence of a functional network allowing mutual complementation of certain actin-binding proteins.
Witke
W
W
Max Planck Institute for Biochemistry, Martinsried, Federal Republic of Germany.
Schleicher
M
M
Noegel
A A
AA
D008841:Actin Cytoskeleton / Q000502:physiology* / Q000648:ultrastructure; D000185:Actinin / Q000235:genetics; D000199:Actins / Q000235:genetics* / Q000502:physiology; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics; D002465:Cell Movement; D002633:Chemotaxis; D003599:Cytoskeleton / Q000502:physiology; D004023:Dictyostelium / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D005822:Genetic Vectors; D008840:Microfilament Proteins / Q000235:genetics; D008954:Models, Biological; D016296:Mutagenesis; D010587:Phagocytosis; D010873:Pinocytosis
D000199:Actins; D002352:Carrier Proteins; D008840:Microfilament Proteins; D000185:Actinin; C060680:abpC protein, Dictyostelium