Matthew L. Wohlever

ALS mutations disrupt self-association between the Ubiquilin Sti1 hydrophobic groove and internal placeholder sequences

This study presents the first crystal structure of the Ubiquilin Sti1 domain bound to a transmembrane domain, showing that ALS mutations disrupt their interaction and reveal internal placeholder sequences that regulate phase separation.

Overcoming Fluorescence Loss in mEOS-based AAA+ Unfoldase Reporters Through Covalent Linkage

The paper develops a method to use mEOS-based reporters for membrane-associated AAA+ unfoldases by covalently linking mEOS to a degron via Sortase, preserving fluorescence and enabling functional analysis.

An Msp1-Protease Chimera Captures Transient AAA+ Interactions and Unveils Ost4 Mislocalization Errors

This study creates an Msp1-protease chimera to capture transient AAA+ interactions, identifies Ost4 as a novel Msp1 substrate, and reveals mislocalization errors in Ost4.

A suite of pre-assembled, pET28b-based Golden Gate vectors for efficient protein engineering and expression

The paper develops a suite of pre-assembled Golden Gate vectors for efficient protein expression and purification in E. coli, enabling customizable and high-throughput protein engineering.

Energetic requirements and mechanistic plasticity in Msp1-mediated substrate extraction from lipid bilayers

This study investigates how Msp1 uses ATP hydrolysis to extract transmembrane helices from lipid bilayers, finding a non-linear relationship between ATP hydrolysis and extraction efficiency.

Yeast de novo proteins integrate into cellular systems using ancient protein targeting and degradation pathways

This study investigates how de novo proteins in yeast integrate into cellular systems using ancient targeting and degradation pathways, revealing a conserved molecular signature that enables their ER localization and regulation.

E3 ligase recruitment by UBQLN2 protects substrates from proteasomal degradation

This study shows UBQLN2 stabilizes substrates by recruiting E3 ligases, which promotes phase separation and protects against proteasomal degradation, and this mechanism is disrupted in ALS mutants.