Ribosomal modifications are associated with mesenchymal fate selection in the neural crest lineage

I Irina Poverennaya A Aliia Murtazina L Lei Li L Lorena Maili L Lukas Sourada L Luis Fernando Montano-Gutierrez R Rozalina Galimullina T Tobias Steinschaden M Markéta Kaiser T Tomáš Zikmund A Adna Goralija T Teng Gao A Aurore Attina O Ornella Clara C Christoph Bartenhagen A Alek Erickson Y Yaakov Gershtein S Shiyuan Chen K Kristyna Polaskova J Jaroslav Štěrba B Bettina Semasch E Emma R. Anderson V Varsha Prakash T Theresa Vincent M Maria Arceo P Per Kogner (Department of Women’s and Children’s Health, Karolinska Institutet) S Susanne Schlisio (Department of Oncology and Pathology, Karolinska Institutet) P Peter V. Kharchenko A Alexandre David J Jozef Kaiser M Matthias Fischer J Jan Skoda P Paul A. Trainor (Stowers Institute for Medical Research) A Andrei S. Chagin (Centre for Bone and Arthritis Research, Institute of Medicine at the Sahlgrenska Academy, University of Gothenburg) I Igor Adameyko

Abstract

Abstract Neural crest cells contribute to craniofacial formation by differentiating into skeletogenic mesenchyme and neuro-glial lineages. Using Smart-seq2 single-cell transcriptomics, we show that mesenchymal fate commitment correlates specifically with the expression of rRNA-modifying and ribosome assembly factors, rather than structural ribosomal proteins. Notably, EMG1 and NHP2 introduce key post-transcriptional modifications into 18S rRNA, including m¹acp³ψ at U1248, which requires TSR3 for final maturation. Disrupting NHP2 or TSR3 in vitro and in vivo perturbs cranial neural crest differentiation; post-migratory temporal knockout of Polr1a or Polr1c also causes craniofacial malformations. These findings align with cell type-specific m¹acp³ψ levels during neural crest differentiation. Given the neural crest contribution to neuroblastoma, we analyze patient data to find that elevated ribosomal control and rRNA-modifying proteins predict poorer outcomes. Complementary experiments in neuroblastoma cell lines reveal functional roles for TSR3 and WDR74 in mesenchymal-like tumor states. Together, our results link rRNA modifications and ribosome assembly to fate decisions, suggesting ribosomal heterogeneity shapes both normal development and tumor progression.

Article Details

Volume / Issue Vol. 17, Issue 1
Published March 09, 2026
ISSN 2041-1723
Publisher Nature Portfolio

Journal Info

Nature Communications

Nature Portfolio

ISSN: 2041-1723 Open Access Life Sciences

Authors (35)

I

Irina Poverennaya

A

Aliia Murtazina

L

Lei Li

L

Lorena Maili

L

Lukas Sourada

L

Luis Fernando Montano-Gutierrez

R

Rozalina Galimullina

T

Tobias Steinschaden

M

Markéta Kaiser

T

Tomáš Zikmund

A

Adna Goralija

T

Teng Gao

A

Aurore Attina

O

Ornella Clara

C

Christoph Bartenhagen

A

Alek Erickson

Y

Yaakov Gershtein

S

Shiyuan Chen

K

Kristyna Polaskova

J

Jaroslav Štěrba

B

Bettina Semasch

E

Emma R. Anderson

V

Varsha Prakash

T

Theresa Vincent

M

Maria Arceo

P

Per Kogner

Department of Women’s and Children’s Health, Karolinska Institutet

S

Susanne Schlisio

Department of Oncology and Pathology, Karolinska Institutet

P

Peter V. Kharchenko

A

Alexandre David

J

Jozef Kaiser

M

Matthias Fischer

J

Jan Skoda

P

Paul A. Trainor

Stowers Institute for Medical Research

A

Andrei S. Chagin

Centre for Bone and Arthritis Research, Institute of Medicine at the Sahlgrenska Academy, University of Gothenburg

I

Igor Adameyko