bioRxiv Science⌕ Search

Biology subjects

Nikolic, L.

Publications and source records attributed to Nikolic, L..

2 recordsLinked to original sources

A closely related pair of superoxide dismutase isozymes from Staphylococcus aureus show distinct stabilities and proton-exchange dynamics

Changes in biochemical properties, caused by iterative mutations in amino acid sequence, underlie the alterations in protein function over time that underpin the evolutionary process. An example is the switching of an enzymes reliance from one essential metal to an alternative as their catalytic cofactor. We previously described such a neofunctionalisation in Staphylococcus aureus, which altered a superoxide dismutase (SOD) enzyme from being an ancestral manganese-dependent (MnSOD) into an extant isozyme that can equally utilise either manganese or iron, termed cambialism (camSOD). Yet its unclear whether camSOD emergence involved selection solely for cofactor flexibility or whether other biochemical properties also diverged during neofunctionalisation. Here, we have investigated an independent biochemical property of the S. aureus SODs, their structural stability. We demonstrate that the neofunctionalised camSOD exhibits increased stability relative to the ancestral MnSOD. S. aureus camSOD is more resistant to both chemical and thermal unfolding in vitro. Crucially, while both isozymes possess a stable core at the heart of their fold, consisting of regions of the protein localised around the metal cofactor that resist hydrogen-deuterium exchange when exposed to isotopically labelled solvent, this core is larger and more exchange-resistant in camSOD than MnSOD. Thus, during the recent divergence of this SOD pair, two distinct biochemical properties have undergone substantial and rapid evolutionary change. This study paves the way for investigations of the structural and functional relationship between these properties, a SODs metal-preference and stability, and of how these properties were concomitantly selected during neofunctionalisation in the S. aureus lineage.

biochemistry↗

Large-scale bidirectional arrayed genetic screens identify OXR1 and EMC4 as modifiers of α-synuclein aggregation

In Parkinsons disease and other synucleinopathies, -synuclein (-Syn) misfolds and forms Ser129-phosphorylated aggregates (pSyn129). The factors controlling this process are largely unknown. Here, we used arrayed CRISPR-mediated gene activation and ablation to discover new pSyn129 modulators. Using quadruple-guide RNAs (qgRNAs) and Cas9, or an inactive Cas9 version fused to a synthetic transactivator, we ablated 2304 and activated 2428 human genes related to mitochondrial, trafficking and motility function in HEK293 cells. After exposure of cells to -Syn fibrils, pSyn129 signals were recorded by high-throughput fluorescence microscopy and aggregates were identified by image analysis. We found that pSyn129 was increased by activating the mitochondrial protein OXR1, which decreased ATP levels and altered the mitochondrial membrane potential. Instead, pSyn129 was reduced by ablation of the endoplasmic reticulum (ER)-associated protein EMC4, which enhanced ER-driven autophagic flux and lysosomal clearance. OXR1 activation preferentially modulated cellular reactions to fibrils derived from multiple system atrophy (MSA) patients, whereas EMC4 ablation broadly reduced pSyn129 across diverse -Syn polymorphs. These findings were confirmed in human iPSC-derived cortical and dopaminergic neurons, where OXR1 preferentially promoted somatic aggregation and EMC4 reduced both somatic and neuritic aggregates. These results uncover previously unrecognized roles for OXR1 and EMC4 in -Syn aggregation, thereby broadening our mechanistic understanding of synucleinopathies.

neuroscience↗