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  • Maquat and Kurosaki
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Maquat Lab

Normal & Disease-Associated RNA Decay

Illustration of Pioneet Translation Complex

The pioneer translation initiation complex
is functionally distinct from but structurally
overlaps with the steady-state translation
initiation complex. View Enlargement

Research in the Maquat lab focuses on RNA decay pathways, largely in human cells, and their relevance to human diseases. One pathway, called nonsense-mediated mRNA decay (NMD) or mRNA surveillance, surveys all newly synthesized mRNAs during what we call a "pioneer" round of translation. This round of translation involves mRNA that is associated with the cap-binding protein heterodimer CBP80 and CBP20 (and variants thereof). It is distinct from the type of translation that supports the bulk of cellular protein synthesis and that involves a different cap-binding protein, eukaryotic initiation factor (eIF) 4E. As a rule, if translation terminates more than 50-55-nucleotides upstream of an exon−exon junction that is marked by what we call a splicing-dependent “mark” or exon-exon junction complex (EJC), then the mRNA will be subject to NMD. By the time CBP80 and CBP20 have been replaced by eIF4E, the EJC “mark” has been removed so that the mRNA is largely immune to NMD. Studies in progress will significantly advance our understanding of the mRNA-binding proteins, translation factors and nucleases that trigger NMD. Moreover, we are now putting our mechanistic findings to use by designing and developing therapies to abrogate or promote NMD with the goal of lessening the severity of nonsense-generated diseases. A remarkable one-third of inherited or acquired diseases are nonsense-generated.

Read More About Our Lab

Lynne Elizabeth Maquat, Ph.D.

Lynne Elizabeth Maquat, Ph.D.

Principal Investigator

Contact Us

  Maquat Lab
MC 3-8507C
601 Elmwood Ave
Rochester, NY 14642

 (585) 273-5640

  (585) 271-2683