Chad G. Pearson

The paper shows that elevated PCM1, caused by Trisomy 21, mislocalizes E3 ligases, delaying primary ciliogenesis by disrupting centrosome function.

This study shows that SPEF1 stabilizes central microtubules in Tetrahymena cilia, with defects in its absence affecting ciliary structure and function.

This paper introduces Tet Trim-Away, a system for rapid protein degradation in Tetrahymena thermophila, enabling acute depletion and loss-of-function phenotypes.

This study shows that Trisomy 21 reduces ciliary SMO and increases GPR161 in SHH signaling, but extended ciliary maturation normalizes these levels between T21 and D21 cells.

This study shows DNA damage response pathways are essential for multiciliated cell differentiation by enabling centriole amplification through a pseudo-cell cycle mechanism.

This study identifies a pathway involving centriolar satellite proteins and an RNA binding protein that regulate CEP350 mRNA localization to centrosomes and its role in centrosome amplification in breast cancer cells.

This paper identifies ASOs that correct cryptic exon inclusion in SDCCAG8, restoring protein expression in BBS patients.

The paper investigates how Big1 regulates cell size by controlling basal body number through cell cycle progression in Tetrahymena.

The paper identifies Unkempt as a key RNA-binding protein promoting local translation at centrosomes during Plk4-induced centriole overduplication.

The paper uses cryo-electron tomography to reveal the structure of cilium inner junctions and shows how protein distribution affects structural stability and assembly.

This paper introduces OINC-seq, a method to quantify subcellular RNA localization through direct oxidation detection, and demonstrates its application in various cellular compartments and live zebrafish.

This study identifies Poc1 as a basal body protein that stabilizes triplet microtubules and interconnections, enhancing resistance to ciliary forces.