CENTROSOME

Updated 05-May-2020.

Mondo shtuff from around the internet, all about CENTROSOME!

Centrosome-associated RNA in surf clam oocytes: Centrosomes are the major microtubule-organizing center in animal cells. They are composed of a pair of [9(3) + 0] centrioles surrounded by a relatively ill-defined pericentriolar matrix, provide the ciliary centriole-kinetosome (basal body) progenitor, and organize the assembly of microtubules into the mitotic spindle during cell division. Despite >100 years of microscopic observation and their obvious significance, our understanding of centrosome composition, dynamic organization, and mechanism of action is limited when compared with that of other cellular organelles. Centrosomes duplicate only once per cell cycle to ensure development of a normal bipolar spindle. The initial event in centrosome duplication is centriole replication, which is generative, semiconservative, and independent of the nucleus. Such observations led to the proposal that centrosomes contain their own complement of nucleic acids, possibly representative of an organellar genome comparable with those described for mitochondria and chloroplasts. The consensus in the field is that centrosomes lack DNA but may contain RNA. We isolated centrosomes from oocytes of the surf clam, Spisula solidissima, and purified from them a unique set of RNAs. We show here by biochemical means and subcellular in situ hybridization that the first transcript we analyzed is intimately associated with centrosomes. Sequence analysis reveals that this centrosome-associated RNA encodes a conserved RNA-directed polymerase domain. The hypothesis that centrosomes contain an intrinsic complement of specific RNAs suggests new opportunities to address the century-old problem of centrosome function, heredity, and evolution.

Abnormal Centrosome Amplification in the Absence of p53: The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.

Centrosome amplification drives chromosomal instability in breast tumor development: Earlier studies of invasive breast tumors have shown that 60-80% are aneuploid and ≈80% exhibit amplified centrosomes. In this study, we investigated the relationship of centrosome amplification with aneuploidy, chromosomal instability, p53 mutation, and loss of differentiation in human breast tumors. Twenty invasive breast tumors and seven normal breast tissues were analyzed by fluorescence in situ hybridization with centromeric probes to chromosomes 3, 7, and 17. We analyzed these tumors for both aneuploidy and unstable karyotypes as determined by chromosomal instability. The results were then tested for correlation with three measures of centrosome amplification: centrosome size, centrosome number, and centrosome microtubule nucleation capacity. Centrosome size and centrosome number both showed a positive, significant, linear correlation with aneuploidy and chromosomal instability. Microtubule nucleation capacity showed no such correlation, but did correlate significantly with loss of tissue differentiation. Centrosome amplification was detected in in situ ductal carcinomas, suggesting that centrosome amplification is an early event in these lesions. Centrosome amplification and chromosomal instability occurred independently of p53 mutation, whereas p53 mutation was associated with a significant increase in centrosome microtubule nucleation capacity. Together, these results demonstrate that independent aspects of centrosome amplification correlate with chromosomal instability and loss of tissue differentiation and may be involved in tumor development and progression. These results further suggest that aspects of centrosome amplification may have clinical diagnostic and/or prognostic value and that the centrosome may be a potential target for cancer therapy.

Centrosome Loss in the Evolution of Planarians: The centrosome, a cytoplasmic organelle formed by cylinder-shaped centrioles surrounded by a microtubule-organizing matrix, is a hallmark of animal cells. The centrosome is conserved and essential for the development of all animal species described so far. Here, we show that planarians, and possibly other flatworms, lack centrosomes. In planarians, centrioles are only assembled in terminally differentiating ciliated cells through the acentriolar pathway to trigger the assembly of cilia. We identified a large set of conserved proteins required for centriole assembly in animals and note centrosome protein families that are missing from the planarian genome. Our study uncovers the molecular architecture and evolution of the animal centrosome and emphasizes the plasticity of animal cell biology and development.

My botty best at summarizing from Wikipedia: the centrosome is thought to have evolved only in the metazoan lineage of eukaryotic cells . it is not essential in certain fly and flatworm species . centrosome contains centrin, cenexin and tektin . mother centriole also has a central role in making cilia and flagella . Aberrant numbers of centrosomes in a cell have been associated with cancer . aberrant numbers are associated with the formation of cancer cells . the mitotic spindle then forms between the two . centrosome doubling does not occur by template reading and assembly . centrioles are not required for the progression of mitosis . when the centrioles are irradiated by a laser, fruit fly Drosophila is largely normal when centrioles are absent . this is due to a mutation in a gene required for their duplication . microtubules of the spindle are focused centrosomes are defective in spindle positioning and in the ability to establish a central localization site in cytokinesis . some cell types arrest in the following cell cycle when centrosoms are absent . in human reproduction, the sperm supplies the centriole that creates the centrosome and microtubule system of the zygote . this initial observation was subsequently extended to many types of human tumors centrosome-related bodies (CRBs) are observed in ectopic places . both enlarged centrosoms and CRBs are similar to tumors . structures can be induced in culture cells by over the presence of an excess of centrosomes is a common event in human tumors . loss of tumor-suppressor p53 produces superfluous centrosoms, as well as deregulating other proteins implica there are two main subfamilies of centrins, both of which are present in the early-branching eukaryote Giardia intestinalis . a failure in cell division could increase centr no studies have been published on the evolution of the pericentriolar material . centrosomes have no recognizable homologs in archea and bacteria . they are part of the “eukaryotic signature genes research shows centrosomes do not contain their own DNA-based genomes . RNA molecules associate with centrosoms, but sequences still found within nucleus . one identified RNA sequence contains a putative centrosomes can form de novo after having been removed (e.g. by laser irradiation) from normal cells.