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Non-Mendelian inheritance during inbreeding of Ca v 3.2 and Ca v 2.3 deficient mice.
- Source :
-
Scientific reports [Sci Rep] 2020 Oct 02; Vol. 10 (1), pp. 15993. Date of Electronic Publication: 2020 Oct 02. - Publication Year :
- 2020
-
Abstract
- The mating of 77 heterozygous pairs (Ca <subscript>v</subscript> 3.2[+|-] x Ca <subscript>v</subscript> 3.2[+|-]) revealed a significant deviation of genotype distribution from Mendelian inheritance in weaned pups. The mating of 14 pairs (Ca <subscript>v</subscript> 3.2[-|-] female x Ca <subscript>v</subscript> 3.2[+|-] male) and 8 pairs (Ca <subscript>v</subscript> 3.2[+|-] female x Ca <subscript>v</subscript> 3.2[-|-] male) confirmed the significant reduction of deficient homozygous Ca <subscript>v</subscript> 3.2[-|-] pups, leading to the conclusion that prenatal lethality may occur, when one or both alleles, encoding the Ca <subscript>v</subscript> 3.2T-type Ca <superscript>2+</superscript> channel, are missing. Also, the mating of 63 heterozygous pairs (Ca <subscript>v</subscript> 2.3[+|-] x Ca <subscript>v</subscript> 2.3[+|-]) revealed a significant deviation of genotype distribution from Mendelian inheritance in weaned pups, but only for heterozygous male mice, leading to the conclusion that compensation may only occur for Ca <subscript>v</subscript> 2.3[-|-] male mice lacking both alleles of the R-type Ca <superscript>2+</superscript> channel. During the mating of heterozygous parents, the number of female mice within the weaned population does not deviate from the expected Mendelian inheritance. During prenatal development, both, T- and R-type Ca <superscript>2+</superscript> currents are higher expressed in some tissues than postnatally. It will be discussed that the function of voltage-gated Ca <superscript>2+</superscript> channels during prenatal development must be investigated in more detail, not least to understand devastative diseases like developmental epileptic encephalopathies (DEE).
Details
- Language :
- English
- ISSN :
- 2045-2322
- Volume :
- 10
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Scientific reports
- Publication Type :
- Academic Journal
- Accession number :
- 33009476
- Full Text :
- https://doi.org/10.1038/s41598-020-72912-9