Reh1 is Required for Nonfunctional 25S RNA Decay

Area of Science:

• Molecular Biology
• Ribosome Biogenesis
• RNA Surveillance

Background:

• Nonfunctional RNA decay (NRD) removes 60S ribosomal subunits with inactivating RNA mutations.
• The mechanism for identifying these defective subunits remained unclear.
• The zinc-finger protein Reh1 was recently identified as the final assembly factor released from nascent 60S subunits.

Purpose of the Study:

• To investigate the role of Reh1 in the degradation of 25S NRD substrates.
• To determine the specificity of Reh1-mediated surveillance for ribosomal RNA mutations.

Main Methods:

• Utilized yeast models to study the impact of Reh1 deletion on the stability of mutated 25S rRNAs.
• Assessed the effect of specific 25S rRNA mutations (A2820G, U2954A) and L1 stalk truncation on ribosome stability and viability.
• Examined the influence of Reh1 deletion on the levels of defective 18S rRNA.

Main Results:

• Reh1 is essential for the degradation of 25S NRD substrates in yeast.
• Mutations in the catalytic center of 25S rRNA are unstable in wild-type cells but stabilized upon REH1 deletion.
• Reh1-mediated surveillance is specific, failing to recognize ribosomes with truncated L1 stalks or defective 18S rRNA.

Conclusions:

• Reh1 acts as a specific surveillance factor targeting 60S ribosomal subunits with mutations near the catalytic center.
• The 25S NRD pathway, mediated by Reh1, demonstrates specificity for certain types of ribosomal defects.
• Yeast lacks a broad surveillance system for all types of mutant ribosomes, such as those with L1 stalk defects.