Christian R. Landry

The paper uses deep mutational scanning to analyze resistance mutations in Fks1, revealing distinct resistance landscapes for echinocandins and triterpenoids, including a novel triterpenoid-specific hotspot.

This study uses population genomics and machine learning to identify genetic markers predictive of antifungal resistance in Candida albicans, highlighting the need for expanded resistance catalogues.

This study shows that gene duplication can lead to non-optimal expression levels that still confer a fitness advantage in yeast.

The paper identifies that peptide hydrophobicity affects their availability in yeast cells, impacting synthetic interaction strength beyond in vitro measurements.

This paper develops a heterologous expression system in yeast to rapidly test and discover resistance-conferring mutations from multiple pathogenic fungi.

The study shows that regulatory mutations cannot drive adaptation to 5-FC in yeast due to the flat fitness function around wild-type expression levels.

The paper shows that resistance mutations to antifungal drugs are conserved across fungal species but epistasis limits their transferability.

This paper trains a machine learning model to predict antifolate resistance mutations in Pneumocystis jirovecii using experimental data and computational modeling, finding mutations that confer resistance to trimethoprim-sulfamethoxazole.

The paper identifies key residues in Fks hotspots that confer echinocandin resistance in Saccharomyces cerevisiae using molecular dynamics and deep-mutational scanning.

The paper introduces a protein-fragment complementation assay to evaluate scaffold efficiency in yeast and identifies key factors affecting it.

The paper examines how molecular interactions and activity-fitness functions determine phenotypic dominance in homomeric proteins.

gyoza is a Snakemake workflow that simplifies the analysis of deep-mutational scanning data into functional impact scores with quality control and reporting.

The paper investigates how Erg3 loss-of-function contributes to echinocandin resistance in Candida species by analyzing combined mutations in ERG3 and FKS2.

The paper curates AMR mutations in fungi to create FungAMR, identifies universal resistance mutations, and provides a tool to screen genomes for AMR mutations.

The paper measures how mutations in residues near an SH3-binding motif affect binding strength in vivo and proposes a model involving interactions outside the canonical binding pocket.

The paper shows that paralog interference enhances negative selection on loss-of-function mutations, preserving genetic redundancy over longer timescales.

The paper presents a cost-effective method for constructing barcoded libraries for genes of any length using low-cost DNA synthesis and standard cloning technologies.

This study investigates the evolution and inhibition of FIKK kinases in P. falciparum, showing they can be inhibited by a single compound.

The paper shows that mutations in protein binding domains, combined with regulatory divergence, determine the fate of gene duplicates in a protein interaction network.

The paper identifies co-translational assembly as a mechanism promoting homomerization of paralogs, which enhances their functional divergence.

This study investigates the role of REV1, an error-prone polymerase, in DNA damage and antifungal drug resistance in Candida albicans, finding that its deletion increases mutation rates and resistance.

The paper shows that hybrid yeast adaptation is slowed by Haldane's sieve due to slower loss of heterozygosity and incomplete dominance of adaptive mutations.

The paper evaluates 4,000 Erg11 variants to determine azole resistance and fitness costs, finding 33% resistance, 88% cross-resistance, and minimal fitness cost.

The paper quantifies the fitness cost of spurious phosphorylation in yeast by expressing tyrosine kinases and analyzing phosphoproteomes, finding a strong correlation between spurious phosphorylation and decreased growth.

The paper duplicates and evolves an homodimeric enzyme to show that compensatory mutations can lead to functional heteromers through subfunctionalization.

The paper shows that mutational biases can lead to the neutral evolution of heteromeric protein complexes over homomeric ones after gene duplication.

This study identifies two distinct pathways for resistance to the antifungal 5-FC in yeast, showing that ecological factors influence which resistance mechanisms dominate.

The paper analyzes TE load in yeast hybrids using long-read sequencing and in vivo assays, finding that transposition rates are not increased by hybridization but are influenced by genotype-specific factors.

This study investigates how hybridization in yeast leads to mitochondrial DNA degeneration and metabolic shifts through large-scale deletions and loss of respiratory function.

The paper identifies a new protein, MTALTND4, encoded by an alternative ATG in the human mitochondrial nd4 gene, which affects mitochondrial bioenergetics.