The sulfotransferase XB5850668.L is required to apportion embryonic ectodermal domains.


Journal

Developmental dynamics : an official publication of the American Association of Anatomists
ISSN: 1097-0177
Titre abrégé: Dev Dyn
Pays: United States
ID NLM: 9201927

Informations de publication

Date de publication:
Dec 2023
Historique:
revised: 08 06 2023
received: 04 04 2023
accepted: 26 07 2023
medline: 4 12 2023
pubmed: 19 8 2023
entrez: 19 8 2023
Statut: ppublish

Résumé

Members of the sulfotransferase superfamily (SULT) influence the activity of a wide range of hormones, neurotransmitters, metabolites and xenobiotics. However, their roles in developmental processes are not well characterized even though they are expressed during embryogenesis. We previously found in a microarray screen that Six1 up-regulates LOC100037047, which encodes XB5850668.L, an uncharacterized sulfotransferase. Since Six1 is required for patterning the embryonic ectoderm into its neural plate, neural crest, preplacodal and epidermal domains, we used loss- and gain-of function assays to characterize the role of XB5850668.L during this process. Knockdown of endogenous XB5850668.L resulted in the reduction of epidermal, neural crest, cranial placode and otic vesicle gene expression domains, concomitant with neural plate expansion. Increased levels had minimal effects, but infrequently expanded neural plate and neural crest gene domains, and infrequently reduced cranial placode and otic vesicle gene domains. Mutation of two key amino acids in the sulfotransferase catalytic domain required for PAPS binding and enzymatic activity tended to reduce the effects of overexpressing the wild-type protein. Our analyses indicates that XB5850668.L is a member of the SULT2 family that plays important roles in patterning the embryonic ectoderm. Some aspects of its influence likely depend on sulfotransferase activity.

Sections du résumé

BACKGROUND BACKGROUND
Members of the sulfotransferase superfamily (SULT) influence the activity of a wide range of hormones, neurotransmitters, metabolites and xenobiotics. However, their roles in developmental processes are not well characterized even though they are expressed during embryogenesis. We previously found in a microarray screen that Six1 up-regulates LOC100037047, which encodes XB5850668.L, an uncharacterized sulfotransferase.
RESULTS RESULTS
Since Six1 is required for patterning the embryonic ectoderm into its neural plate, neural crest, preplacodal and epidermal domains, we used loss- and gain-of function assays to characterize the role of XB5850668.L during this process. Knockdown of endogenous XB5850668.L resulted in the reduction of epidermal, neural crest, cranial placode and otic vesicle gene expression domains, concomitant with neural plate expansion. Increased levels had minimal effects, but infrequently expanded neural plate and neural crest gene domains, and infrequently reduced cranial placode and otic vesicle gene domains. Mutation of two key amino acids in the sulfotransferase catalytic domain required for PAPS binding and enzymatic activity tended to reduce the effects of overexpressing the wild-type protein.
CONCLUSIONS CONCLUSIONS
Our analyses indicates that XB5850668.L is a member of the SULT2 family that plays important roles in patterning the embryonic ectoderm. Some aspects of its influence likely depend on sulfotransferase activity.

Identifiants

pubmed: 37597164
doi: 10.1002/dvdy.648
doi:

Substances chimiques

Sulfotransferases EC 2.8.2.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1407-1427

Subventions

Organisme : NIDCR NIH HHS
ID : R01 DE026434
Pays : United States

Informations de copyright

© 2023 American Association for Anatomy.

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Auteurs

Alexander Marchak (A)

Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

Karen M Neilson (KM)

Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

Himani D Majumdar (HD)

Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

Kiyoshi Yamauchi (K)

Department of Biological Science, Shizuoka University, Shizuoka, Japan.

Steven L Klein (SL)

Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

Sally A Moody (SA)

Department of Anatomy and Cell Biology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia, USA.

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