Abstract
Stress granules (SGs) are cytoplasmic foci that appear in cells exposed to stress-induced translational inhibition. SGs function as a triage center, where mRNAs are sorted for storage, degradation, and translation reinitiation. The underlying mechanisms of SGs dynamics are still being characterized, although many key players have been identified. The main components of SGs are stalled 48S preinitiation complexes. To date, many other proteins have also been found to localize in SGs and are hypothesized to function in SG dynamics. Most recently, the microtubule cytoskeleton and associated motor proteins have been demonstrated to function in SG dynamics. In this paper, we will discuss current literature examining the function of microtubules and the molecular microtubule motors in SG assembly, coalescence, movement, composition, organization, and disassembly.
Highlights
Stress granules (SGs) are nonmembranous cytoplasmic foci that rapidly appear in cells exposed to various types of stress including oxidative stress, heat shock, viral infection, and UV irradiation, all of which impair translation initiation
We will discuss the importance of the microtubule network and the microtubule motors involved in SG dynamics including the assembly, coalescence, and disassembly processes
These results indicate that SG formation is part of a cell’s native physiological response, rather than an in vitro artifact of cell culture systems
Summary
Stress granules (SGs) are nonmembranous cytoplasmic foci that rapidly appear in cells exposed to various types of stress including oxidative stress, heat shock, viral infection, and UV irradiation, all of which impair translation initiation (as reviewed in [1,2,3]) In response to such cellular insults, the cell activates mechanisms to selectively repress the translation of house-keeping gene transcripts to conserve energy for repair of stress-induced damage, while upregulating translation of proteins required for the repair process such as DNA-repair proteins, chaperone proteins, and transcription factors (as reviewed in [3,4,5,6]). The eIF2/eIF5 deficient “stalled” 48S preinitiation complexes consisting of bound polyadenylated mRNAs, the small ribosomal subunits, as well as various translation initiation factors including eIF3, eIF4E, and eIF4G, are organized into the newly forming SGs [26, 27] These defective 48S preinitiation complexes are critical substrates for the assembly process of SGs to occur [26]. Overexpression alone of specific RNA-binding proteins whose translation is typically repressed [5, 31, 32, 39, 40] or even the inhibition of certain initiation factors results in spontaneous SG formation [5, 41]
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