Confirming the enzymatic activity and neurodevelopmental trajectory of PYCR1 mutation in one child with autosomal-recessive cutis laxa type 2.


Journal

Molecular genetics and genomics : MGG
ISSN: 1617-4623
Titre abrégé: Mol Genet Genomics
Pays: Germany
ID NLM: 101093320

Informations de publication

Date de publication:
22 Aug 2024
Historique:
received: 09 02 2024
accepted: 30 07 2024
medline: 22 8 2024
pubmed: 22 8 2024
entrez: 22 8 2024
Statut: epublish

Résumé

Autosomal-recessive cutis laxa type 2 (ARCL2) is a rare genetic disorder caused by pyrroline-5-carboxylate reductase 1 (PYCR1) mutations and characterized by loose and sagging skin, typical facial features, intrauterine growth retardation, and developmental delay. To study the effect of PYCR1 mutations on protein function and clinical features, we identified a homozygous missense mutation c.559G > A (p.Ala187Thr) in PYCR1 in a Chinese child with typical clinical features, especially severe developmental delays. The three-dimensional (3D) model showed the modification of the hydrogen bonds produce a misfolding in the mutant PYCR1 protein. Mutagenesis and enzyme assay study revealed decreased activity of the mutant protein in vitro, indicating that this mutation impairs PYCR1 function. Our findings confirmed abnormal enzymatic activity and neurodevelopmental trajectory of this PYCR1 mutation.

Identifiants

pubmed: 39172257
doi: 10.1007/s00438-024-02173-y
pii: 10.1007/s00438-024-02173-y
doi:

Substances chimiques

Pyrroline Carboxylate Reductases EC 1.5.1.-
delta-1-Pyrroline-5-Carboxylate Reductase EC 1.5.1.2

Types de publication

Journal Article Case Reports

Langues

eng

Sous-ensembles de citation

IM

Pagination

81

Subventions

Organisme : The Beijing Municipal Administration of Hospitals Incubating Program
ID : PX2023049
Organisme : The Beijing Municipal Administration of Hospitals Incubating Program
ID : PX2020056
Organisme : Clinical Testing research fund of the Capital Institute of Pediatrics
ID : CTR005

Informations de copyright

© 2024. The Author(s).

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Auteurs

Shaofang Shangguan (S)

Department of Medical Genetics, Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China.

Xueyuan Zhang (X)

Department of Children's Nutrition Research Center, Affiliated Children's Hospital of Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China.

Yangyang Ge (Y)

Department of Medical Genetics, Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China.

Ye Han (Y)

Department of Neurology, Affiliated Children's hospital of Capital Institute of Pediatrics, Beijing, China.

Ling Xiao (L)

Department of Children's Nutrition Research Center, Affiliated Children's Hospital of Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China.

Yu Zhang (Y)

Department of Laboratory Center, Capital Institute of Pediatrics, Beijing, China.

Hua Xie (H)

Department of Medical Genetics, Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China.

Xiaoli Chen (X)

Department of Medical Genetics, Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China. xiaolichen@pumc.edu.cn.

Xiaoyan Wang (X)

Department of Children's Nutrition Research Center, Affiliated Children's Hospital of Capital Institute of Pediatrics, Yabao Road, Chaoyang District, Beijing, 100020, China. yanziskyv@126.com.

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