Ribosome profiling of platelets and platelet-like particles (PLPs) demonstrates a role for PELO in mRNA decay. (Top) Megakaryocytes (left) produce platelets that are naturally devoid of PELO protein. Ribosome profiling measurements on platelets demonstrate that thousands of mRNAs are translationally active and that thrombin increases translation of many of these transcripts. Because platelets are anucleate, new mRNAs cannot be made, and their mRNA is degraded over time thus limiting translation. However, because the ribosome rescue factor PELO is naturally absent from platelets, ribosomes remain attached to the 3′ untranslated region (UTR) of platelets and slow their degradation thus potentially prolonging their availability for translation into protein. (Bottom) When PELO is transgenically increased in PLPs from a megakaryocyte cell line (Meg01), ribosomes are removed from the 3′UTR, and mRNA degradation is accelerated, potentially decreasing protein synthesis.

Ribosome profiling of platelets and platelet-like particles (PLPs) demonstrates a role for PELO in mRNA decay. (Top) Megakaryocytes (left) produce platelets that are naturally devoid of PELO protein. Ribosome profiling measurements on platelets demonstrate that thousands of mRNAs are translationally active and that thrombin increases translation of many of these transcripts. Because platelets are anucleate, new mRNAs cannot be made, and their mRNA is degraded over time thus limiting translation. However, because the ribosome rescue factor PELO is naturally absent from platelets, ribosomes remain attached to the 3′ untranslated region (UTR) of platelets and slow their degradation thus potentially prolonging their availability for translation into protein. (Bottom) When PELO is transgenically increased in PLPs from a megakaryocyte cell line (Meg01), ribosomes are removed from the 3′UTR, and mRNA degradation is accelerated, potentially decreasing protein synthesis.

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