Jordan D. Ward

The paper investigates how fluorophore choice and epitope positioning affect the oscillatory behavior of destabilized reporter proteins in C. elegans.

The paper characterizes the binding and functional landscape of NHR-25, a nuclear hormone receptor in C. elegans, revealing two binding modes and the role of a single response element in regulating gene expression.

This study identifies MLT-11 as essential for C. elegans embryogenesis and shows conserved sequences in MLT-11 are critical for cuticle structure.

This study identifies a conserved signaling module involving LIN-42 and KIN-20 that regulates molting timing in C. elegans, mirroring the mammalian PER-CK1 complex.

The paper develops a toolkit for fluorescently tagging apical extracellular matrix components in C. elegans to study their molecular architecture and spatial organization.

The paper identifies spia-1 as a gene involved in immune activation in C. elegans by sensing cuticle damage through its secreted protein with a novel cysteine-cradle domain.

This paper introduces a C. elegans model of progeria by mutating baf-1 to mimic the human NGPS mutation, showing accelerated aging and altered gene expression.

This study identifies mlt-11 as an NHR-23 target gene essential for C. elegans cuticle structure and function, showing its role in patterning cuticle layers and maintaining barrier integrity.

This paper shows that NHR-23 is essential for C. elegans development and apical extracellular matrix structure by regulating gene expression in seam and hypodermal cells.

This study investigates the role of lin-42 and kin-20 in the circadian clock of C. elegans using a bioluminescence reporter, showing they regulate the period length through neuronal cells.

The paper optimizes experimental parameters and provides new reagents for studying C. elegans lysosomal proteins, addressing challenges like protein degradation and detection.

The paper identifies distinct gene regulation by NHR-23 and SPE-44 during C. elegans spermatogenesis and shows their combined depletion affects additional genes.

The paper introduces the mIAA7 degron, which enhances auxin-mediated protein degradation efficiency in C. elegans, with some improvements in leakiness when combined with the C.e.AID2 system.

This study identifies MLT-11, a protease inhibitor essential for C. elegans molting and embryogenesis, showing its role in aECM remodeling and cuticle integrity.

The paper introduces an engineered auxin analog and AtTIR1(F79G) pair to improve the specificity and efficacy of the auxin degradation system in C. elegans.

The paper introduces new tools for the auxin-inducible degron system in C. elegans, enabling conditional protein depletion through CRISPR/Cas9-mediated genome editing.

This study identifies NHR-23/NR1F1 as a critical regulator of spermatogenesis in C. elegans, functioning downstream of the sex determination pathway and independent of the SPE-44 network.

This paper improves the AID system in C. elegans for single-cell protein degradation using NAA and demonstrates its application in developmental studies.

The paper shows that the glucocorticoid receptor ligand-binding domain can control protein activity in C. elegans using a heterologous gene expression system.