Centrosome and microtubule instability in aging Drosophila cells

Several cytoskeletal changes are associated with aging which includes alter ations in muscle structure leading to muscular atrophy, and weakening of th e microtubule network which affects cellular secretion and maintenance of c ell shape. Weakening of the microtubule network during meiosis in aging ooc ytes can result in aneuploidy or trisomic zygotes with increasing maternal age. Imbalances of cytoskeletal organization can lead to disease such as Al zheimer's, muscular disorders, and cancer. Because many cytoskeletal diseas es are related to age we investigated the effects of aging on microtubule o rganization in cell cultures of the Drosophila cell model system (Schneider S-1 and Kc23 cell lines). This cell model is increasingly being used as an alternative system to mammalian cell cultures. Drosophila cells are amenab le to genetic manipulations and can be used to identify and manipulate gene s which are involved in the aging processes. Immunofluorescence, scanning, and transmission electron microscopy were employed for the analysis of micr otubule organizing centers (centrosomes) and microtubules at various times after subculturing cells in fresh medium. Our results reveal that centrosom es and the microtubule network becomes significantly affected in aging cell s after 5 days of subculture. At 5-14 days of subculture, 1% abnormal out o f 3% mitoses were noted which were clearly distinguishable from freshly sub cultured control cells in which 3% of cells undergo normal mitosis with bip olar configurations. Microtubules are also affected in the midbody during c ell division. The midbody in aging cells becomes up to 10 times longer when compared with midbodies in freshly subcultured cells. During interphase, m icrotubules are often disrupted and disorganized, which may indicate improp er function related to transport of cell organelles along microtubules. The se results are likely to help explain some cytoskeletal disorders and disea ses related to aging. J. Cell. Biochem. 74:229-241, 1999. (C) 1999 Wiley-Li ss, Inc.