Philippe Bastin

This study shows trypanosomatids use homodimeric kinesin-2 motors KIN2A and KIN2B for intraflagellar transport, with KIN2B being essential and KIN2A having a more limited role.

The paper shows that Wnt and Nodal asymmetries contribute to left-right asymmetry in mice despite the absence of node flow, suggesting a novel mechanism for symmetry breaking.

The paper investigates the role of IFT-A in anterograde intraflagellar transport in Trypanosoma brucei, finding that IFT140 is essential for train assembly.

This study investigates the role of CCDC40 in trypanosome flagellum structure and function, revealing that its depletion causes structural defects but not impaired cell division.

This study reveals how intraflagellar transport (IFT) trains selectively associate with specific microtubules in Trypanosoma brucei flagella using advanced microscopy techniques.

The paper develops a mass spectrometry pipeline to quantify tubulin polyglutamylation in Trypanosoma brucei flagella, identifying novel glutamylation sites and crosstalk with detyrosination.

This study uses tagged tubulin to show that Trypanosoma brucei restricts microtubule assembly to the new flagellum during duplication but allows transient reassembly in mature flagella after cell division.

The paper identifies ANKS3/BICC1 as a post-transcriptional regulator of NPHP1 transcripts, linking it to ciliopathy phenotypes through transcript decay and ciliary dysfunction.

This study uses scRNA-seq to analyze Trypanosoma brucei development in tsetse fly salivary glands, revealing dynamic VSG gene activation and monoallelic expression establishment.

The paper identifies biallelic LRRC56 mutations causing ciliary dysfunction and laterality defects in two families, linking LRRC56 to intraflagellar transport and dynein arm assembly.