Cellular stress and RNA splicing.
In response to physical and chemical stresses that affect protein folding and, thus, the execution of normal metabolic processes, cells activate gene-expression strategies aimed at increasing their chance of survival. One target of several stressing agents is pre-mRNA splicing, which is inhibited upon heat shock. Recently, the molecular basis of this splicing inhibition has begun to emerge. Interestingly, different mechanisms seem to be in place to block constitutive pre-mRNA splicing and to affect alternative splicing regulation. This could be important to modulate gene expression during recovery from stress. Thus, pre-mRNA splicing emerges as a central mechanism to integrate cellular and metabolic stresses into gene-expression profiles.
Biamonti
Giuseppe
G
Istituto di Genetica Molecolare-Consiglio Nazionale delle Ricerche Via Abbiategrasso 207, 27100 Pavia, Italy. biamonti@igm.cnr.it
Caceres
Javier F
JF
D000818:Animals; D018797:Cell Cycle Proteins / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D009363:Neoplasm Proteins / Q000378:metabolism; D012322:RNA Precursors / Q000378:metabolism; D012326:RNA Splicing / Q000235:genetics / Q000502:physiology*; D016601:RNA-Binding Proteins / Q000378:metabolism; D012097:Repressor Proteins / Q000378:metabolism; D000068103:Serine-Arginine Splicing Factors; D013312:Stress, Physiological / Q000502:physiology*
D018797:Cell Cycle Proteins; D009363:Neoplasm Proteins; D012322:RNA Precursors; D016601:RNA-Binding Proteins; D012097:Repressor Proteins; C115188:SRSF10 protein, human; D000068103:Serine-Arginine Splicing Factors