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Temporal and developmental requirements for the Prader-Willi imprinting center
Amanda J DuBose1, Emily Y Smith, Karen A Johnstone
1Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, FL 32610, USA.
Summary
The Prader-Willi syndrome imprinting center (PWS-IC) is crucial for paternal gene expression in early embryos. However, it becomes unnecessary for maintaining imprinted gene status in the developing brain.
Area of Science:
- Genetics
- Developmental Biology
- Epigenetics
Background:
- Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are neurodevelopmental disorders caused by disruptions in imprinted gene expression.
- Two imprinting centers, PWS-IC and AS-IC, regulate these imprinted genes, with PWS-IC activating paternal-specific transcription.
Purpose of the Study:
- To investigate the developmental role of the PWS-IC.
- To determine when the PWS-IC is essential for maintaining imprinted gene expression.
Main Methods:
- Creation of a conditional PWS-IC allele.
- Deletion of the paternal PWS-IC at different developmental stages (pre-implantation and early brain progenitors).
- Analysis of paternal-only gene expression in the neonatal brain.
Main Results:
- Deletion of the paternal PWS-IC before implantation abolished paternal-only gene expression in the neonatal brain.
- Deletion of the PWS-IC in early brain progenitors did not affect the imprinted status of PWS/AS genes in newborns.
- The PWS-IC is essential for protecting the paternal epigenotype at the epiblast stage.
Conclusions:
- The PWS-IC is critical for establishing paternal imprinting in early development.
- The PWS-IC's function in maintaining imprinting is dispensable after the epiblast stage.
Related Concept Videos
01:22Imprinting
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02:30Genomic Imprinting and Inheritance
Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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