THE CYTOSKELETON IN SPACEFLOWN CELLS: AN OVERVIEW

Cytoskeletal changes in spaceflown cells include altered actin and tubulin polymerization; morphological anomalies in actin stress fibers, microtubules, and intermediate filament networks; coalesced, shortened microtubules; loss of microtubule-cell membrane contact; perinuclear cytokeratin network loosening; disruption of microtubule organizing centers; and centrosome complex anomalies during cell division. Cellular function depends on interaction of actin stress fibers, microtubules and intermediate filaments with complex assemblies of hundreds of cytoskeletal accessory binding proteins. Thus, spaceflightinduced cytoskeletal changes may affect cell shape, mechanical support, cell movement, transport and position of RNA, protein kinase C (PKC) and other cellular proteins, chromosome segregation during mitosis, and in plants, cytoplasmic streaming and polarized growth and orientation regulated by actin binding proteins. In lymphocytes, microtubules disrupted by launch vibration appear to reorganize in microgravity but may not be typical. Cells adapt to mechanical stimuli by modifying cytoskeletal structure and regulating signal transduction through membrane inositol phospholipid interactions with cytoskeletal proteins such as gelsolin. Gelsolin links cytoskeletal dynamics (actin polymerization) to signal transduction at the cell inner membrane. We found gelsolin precursor message downregulation in cDNA microarray assays of lymphocytes flown on the space shuttle. Of over 20,000 genes evaluated, eleven cytoskeleton-related genes were expressed differently in flown compared to ground controls. I postulate that signal transduction at the inner membrane, through the interaction of actin polymerizing proteins and inositol phosphate hydrolysis mediated by cytoskeleton binding proteins, is a mechanism for reduced cell growth in space.