PubMed · 15955582
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Ana Otero, Ken Goto. 2005. Microalgae: the "self-synchronized" eukaryotes.. https://doi.org/10.1016/j.tibtech.2005.05.014
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Recent years have seen a revival of interest in the possible contribution of centrosomes to the development of human cancers. The underlying hypothesis, formulated almost 100 years ago (Boveri T. The origin of malignant tumors; Baltimore, MD: Williams and Wilkins, 1929.), states that numerical and/or structural centrosome abnormalities will cause chromosome [corrected] missegregation. In addition, centrosome abnormalities are expected to affect cell shape, polarity, and motility. Thus, deregulation of centrosome number and function may foster both chromosomal instability and loss of tissue architecture--2 of the most common phenotypes associated with solid human tumors. In support of the role of centrosome deregulation in tumorigenesis, centrosome aberrations have been observed in early, premalignant lesions. Moreover, they are frequent in many different types of common tumors and their prominence often correlates with poor clinical outcome. This review addresses the origins of centrosome aberrations in human tumors as well as the expected impact of centrosome aberrations on cell fate and tumor development.
We investigated the effects of two natural dietary retinoid X receptor (RXR) ligands, phytanic acid (PA) and docosahexaenoic acid (DHA), on proliferation and on the metabolism of retinol (vitamin A) in both cultured normal human prostate epithelial cells (PrECs) and PC-3 prostate carcinoma cells. PA and DHA inhibited the proliferation of the parental PC-3 cells and PC-3 cells engineered to overexpress human lecithin:retinol acyltransferase (LRAT) in both the absence and presence of retinol. A synthetic RXR-specific ligand also inhibited PC-3 cell proliferation, whereas all-trans retinoic acid (ATRA) did not. PA and DHA treatment increased the levels of retinyl esters (REs) in both PrECs and PC-3 cells and generated novel REs that eluted on reverse-phase HPLC at 54.0 and 50.5 min, respectively. Mass spectrometric analyses demonstrated that these novel REs were retinyl phytanate (54.0 min) and retinyl docosahexaenoate (50.5 min). Neither PA nor DHA increased LRAT mRNA levels in these cells. In addition, we demonstrate that retinyl phytanate was generated by LRAT in the presence of PA and retinol; however, retinyl docosahexaenoate was produced by another enzyme in the presence of DHA and retinol.
Mycoplasmas are cell wall-less bacteria considered among the smallest and simplest prokaryotes known, and yet several species including Mycoplasma pneumoniae have a remarkably complex cellular organization highlighted by the presence of a differentiated terminal organelle, a membrane-bound cell extension distinguished by an electron-dense core. Adhesin proteins localize specifically to the terminal organelle, which is also the leading end in gliding motility. Duplication of the terminal organelle is thought to precede cell division, but neither the mechanism of its duplication nor its role in this process is understood. Here we used fluorescent protein fusions and time-lapse digital imaging to study terminal organelle formation in detail in growing cultures of M. pneumoniae. Individual cells ceased gliding as a new terminal organelle formed adjacent to an existing structure, which then migrated away from the transiently stationary nascent structure. Multiple terminal organelles often formed before cytokinesis was observed. The separation of terminal organelles was impaired in a nonmotile mutant, indicating a requirement for gliding in normal cell division. Examination of cells expressing two different fluorescent protein fusions concurrently established their relative order of appearance, and changes in the fluorescence pattern over time suggested that nascent terminal organelles originated de novo rather than from an existing structure. In summary, spatial and temporal analysis of terminal organelle formation has yielded insights into the nature of M. pneumoniae cell division and the role of gliding motility in that process.