Bop1 is required to establish precursor domains of craniofacial tissues

Authors

Stephanie Keer, Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Karen M. Neilson, Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Helene Cousin, Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, Massachusetts, USA.
Himani D. Majumdar, Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Dominique Alfandari, Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, Massachusetts, USA.
Steven L. Klein, Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Sally A. Moody, Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

Document Type

Letter to the Editor

Publication Date

11-16-2023

Journal

Genesis (New York, N.Y. : 2000)

DOI

10.1002/dvg.23580

Keywords

Xenopus; branchial arch; neural plate; otic vesicle; preplacodal ectoderm

Abstract

Bop1 can promote cell proliferation and is a component of the Pes1-Bop1-WDR12 (PeBoW) complex that regulates ribosomal RNA processing and biogenesis. In embryos, however, bop1 mRNA is highly enriched in the neural plate, cranial neural crest and placodes, and potentially may interact with Six1, which also is expressed in these tissues. Recent work demonstrated that during development, Bop1 is required for establishing the size of the tadpole brain, retina and cranial cartilages, as well as controlling neural tissue gene expression levels. Herein, we extend this work by assessing the effects of Bop1 knockdown at neural plate and larval stages. Loss of Bop1 expanded neural plate gene expression domains (sox2, sox11, irx1) and reduced neural crest (foxd3, sox9), placode (six1, sox11, irx1, sox9) and epidermal (dlx5) expression domains. At larval stages, Bop1 knockdown reduced the expression of several otic vesicle genes (six1, pax2, irx1, sox9, dlx5, otx2, tbx1) and branchial arch genes that are required for chondrogenesis (sox9, tbx1, dlx5). The latter was not the result of impaired neural crest migration. Together these observations indicate that Bop1 is a multifunctional protein that in addition to its well-known role in ribosomal biogenesis functions during early development to establish the craniofacial precursor domains.

APA Citation

Keer, Stephanie; Neilson, Karen M.; Cousin, Helene; Majumdar, Himani D.; Alfandari, Dominique; Klein, Steven L.; and Moody, Sally A., "Bop1 is required to establish precursor domains of craniofacial tissues" (2023). GW Authored Works. Paper 3797.
https://hsrc.himmelfarb.gwu.edu/gwhpubs/3797

Department

Anatomy and Regenerative Biology