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Presphenoidal synchondrosis fusion in DBA/2J mice
Allysa Adams1, Brandeis McBratney-Owen, Brittany Newby
1Orthopaedic Research Laboratories, Boston Children's Hospital, Boston, MA, USA.
Insights
The presphenoidal synchondrosis (PSS) growth plate closes in DBA/2J mice, unlike other strains. Its closure is genetically complex, influenced by different chromosomal regions depending on the genetic background.
Area of Science:
- Craniofacial development
- Genetics of skeletal growth
- Mouse models in developmental biology
Background:
- Cranial base growth plates are crucial for skull development and facial positioning.
- The presphenoidal synchondrosis (PSS) is a key midline cranial base growth plate.
- Premature or abnormal PSS closure can impact craniofacial structure.
Purpose of the Study:
- To investigate the genetic basis of PSS closure in the DBA/2J mouse strain.
- To determine if PSS closure is a Mendelian trait.
- To identify genetic loci influencing PSS closure.
Main Methods:
- Crossbreeding DBA/2J mice with C57BL/6J and DBA/1J strains.
- Analyzing PSS closure in F1, F1 backcross, and F1 intercross offspring.
- Utilizing genome-wide single nucleotide polymorphism (SNP) arrays to map genetic loci.
Main Results:
- PSS closure is genetically determined in DBA/2J mice.
- The inheritance pattern of PSS closure is not a simple Mendelian trait.
- A specific region on chromosome 11 in C57BL/6J influenced PSS closure frequency, but the homologous region in DBA/1J did not.
Conclusions:
- PSS closure in DBA/2J mice is a complex genetic trait.
- Different genetic loci modify PSS closure depending on the outcross strain (C57BL/6J vs. DBA/1J).
- This complexity highlights the intricate genetic regulation of cranial base development.
Abstract:
Cranial base growth plates are important centers of longitudinal growth in the skull and are responsible for the proper anterior placement of the face and the stimulation of normal cranial vault development. We report that the presphenoidal synchondrosis (PSS), a midline growth plate of the cranial base, closes in the DBA/2J mouse strain but not in other common inbred strains. We investigated the genetics of PSS closure in DBA/2J mice by evaluating F1, F1 backcross, and/or F1 intercross offspring from matings with C57BL/6J and DBA/1J mice, whose PSS remain open. We observed that PSS closure is genetically determined, but not inherited as a simple Mendelian trait. Employing a genome-wide SNP array, we identified a region on chromosome 11 in the C57BL/6J strain that affected the frequency of PSS closure in F1 backcross and F1 intercross offspring. The equivalent region in the DBA/1J strain did not affect PSS closure in F1 intercross offspring. We conclude that PSS closure in the DBA/2J strain is complex and modified by different loci when outcrossed with C57BL/6J and DBA/1J mice.
