Anyone know of any experiments that have knocked out the genes for producing centrioles in a worm, mouse, fish, fly or whatever animal? Are the genes for centrioles even identified? It has been shown that centrosomes form with out centrioles so I'm curious how lack of centrioles would effect the system of an animal as a whole.
One of the chief components of centrosome is γ-Tubulin.
In this study the authors have reported the effect of γ-Tubulin knockout in mice.
Quoting the abstract:
Gamma-tubulin regulates the nucleation of microtubules, but knowledge of its functions in vivo is still fragmentary. Here, we report the identification of two closely related gamma-tubulin isoforms, TUBG1 and TUBG2, in mice, and the generation of TUBG1- and TUBG2-deficient mice. TUBG1 was expressed ubiquitously, whereas TUBG2 was primarily detected in the brain. The development of TUBG1-deficient (Tubg1-/-) embryos stopped at the morula/blastocyst stages due to a characteristic mitotic arrest: the mitotic spindle was highly disorganized, and disorganized spindles showed one or two pole-like foci of bundled MTs that were surrounded by condensed chromosomes. TUBG2 was expressed in blastocysts, but could not rescue the TUBG1 deficiency. By contrast, TUBG2-deficient (Tubg2-/-) mice were born, grew, and intercrossed normally. In the brain of wild-type mice, TUBG2 was expressed in approximately the same amount as TUBG1, but no histological abnormalities were found in the Tubg2-/- brain. These findings indicated that TUBG1 and TUBG2 are not functionally equivalent in vivo, that TUBG1 corresponds to conventional gamma-tubulin, and that TUBG2 may have some unidentified function in the brain.
Another important gene is pericentrin. Fibroblasts from pericentrin knockout mice show abnormal spindles during mitosis have been studied.
In agreement with a model in which pericentrin is required for correct spindle orientation, fibroblasts isolated from PCNT knockout mice show a significant increase in cells with disrupted astral microtubules and misoriented spindles (Fig. 2; unpublished data; Zheng, G., personal communication). Spindle misorientation is shown by an increase in the angle formed by the pole-to-pole spindle vector and the cell–substrate adhesion plane in pericentrin knockout compared with wild-type fibroblasts.
Apparently both TUBG and PCNT deletions (individually) are not lethal.