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Updated: Jul 1, 2026

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Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner
Published on: December 10, 2015
Serdin1/Lrrc10 is dispensable for mouse development
Nikolay L Manuylov1, Ekaterina Manuylova, Valeriya Avdoshina
1Department of Genetics, Dartmouth Medical School, Hanover, New Hampshire, USA.
Summary
Leucine-rich repeat containing 10 (LRRC10) is crucial for zebrafish heart development. However, Lrrc10-null mice show no cardiac defects, indicating divergent roles in mammalian heart development.
Area of Science:
- Developmental Biology
- Genetics
- Cardiovascular Research
Background:
- Serdin1/Lrrc10 encodes a novel cardiac-specific leucine-rich protein.
- Evolutionary conservation suggests a vital role for LRRC10 in cardiac development.
- Zebrafish lrrc10 knockdown models exhibit severe heart looping defects.
Purpose of the Study:
- To investigate the function of Lrrc10 in mammalian cardiac development.
- To determine if Lrrc10 is essential for heart development in mice.
Main Methods:
- Gene disruption of Lrrc10 in mice to create Lrrc10-null models.
- Phenotypic analysis of Lrrc10-null mice during cardiac development.
Main Results:
- Lrrc10-null mice develop normally without any discernible cardiac phenotype.
- This contrasts sharply with the observed defects in zebrafish lrrc10 knockdown models.
Conclusions:
- Lrrc10 function in cardiac development appears to be divergent between zebrafish and mice.
- The essential role of LRRC10 in mammalian heart development requires further investigation.

