Yehonadav Komemy
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Yehonadav Komemy has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Adva Hadar
Weizmann Institute of Science
1 shared publication - Alfredo Isaac Ponce-Arias
Weizmann Institute of Science
1 shared publication - Andrew Flatley
Core Facility Monoclonal Antibodies, Helmholtz Zentrum München, Neuherberg, Germany
1 shared publication - Anna Lilja
Weizmann Institute of Science
1 shared publication - Bidisha Bhattacharya
Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
1 shared publication - Ejona Rusha
Helmholtz Zentrum Munich GmbH
1 shared publication
Latest Publications
- Open Access
RTTN moonlights beyond the centrosome to control ribosome biogenesis and tRNA modification in human brain organoids
RTTN (rotatin) is a centrosomal protein mutated in severe malformations of cortical development, yet how its dysfunction disrupts human corticogenesis has remained unclear. Here, we show that RTTN has an unrecognized function at the core of the translation machinery. Using human telencephalic and hippocampal organoids carrying distinct RTTN alleles, together with single-cell and bulk transcriptomics, polysome profiling, and tRNA pseudouridine sequencing, we find that RTTN is enriched in cycling first-trimester neural progenitors and physically associates with ribosome-biogenesis and RNA-processing factors. RTTN mutations impair rRNA biogenesis and polysome assembly, reduce cytoplasmic ribosome density and nascent protein synthesis, and remodel the tRNA pseudouridylation landscape through both a PUS7L-dependent variable-arm signature and a broader RTTN-specific defect. These translational deficits are accompanied by prolonged mitosis, reduced entry into S-phase, and impaired interkinetic nuclear migration in mutant progenitors. Our findings redefine RTTN as a regulator of ribosome homeostasis and mRNA translation and implicate defective translational capacity as a driver of RTTN-associated microcephaly.
Open AccessRTTN moonlights beyond the centrosome to control ribosome biogenesis and tRNA modification in human brain organoids
RTTN (rotatin) is a centrosomal protein mutated in severe malformations of cortical development, yet how its dysfunction disrupts human corticogenesis has remained unclear. Here, we show that RTTN has an unrecognized function at the core of the translation machinery. Using human telencephalic and hippocampal organoids carrying distinct RTTN alleles, together with single-cell and bulk transcriptomics, polysome profiling, and tRNA pseudouridine sequencing, we find that RTTN is enriched in cycling first-trimester neural progenitors and physically associates with ribosome-biogenesis and RNA-processing factors. RTTN mutations impair rRNA biogenesis and polysome assembly, reduce cytoplasmic ribosome density and nascent protein synthesis, and remodel the tRNA pseudouridylation landscape through both a PUS7L-dependent variable-arm signature and a broader RTTN-specific defect. These translational deficits are accompanied by prolonged mitosis, reduced entry into S-phase, and impaired interkinetic nuclear migration in mutant progenitors. Our findings redefine RTTN as a regulator of ribosome homeostasis and mRNA translation and implicate defective translational capacity as a driver of RTTN-associated microcephaly.