-
Something wrong with this record ?
Prdm9 Intersubspecific Interactions in Hybrid Male Sterility of House Mouse
A. Mukaj, J. Piálek, V. Fotopulosova, AP. Morgan, L. Odenthal-Hesse, ED. Parvanov, J. Forejt
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1983 to 1 year ago
PubMed Central
from 2008
Open Access Digital Library
from 1983-12-01
Open Access Digital Library
from 1983-12-01
Oxford Journals Open Access Collection
from 1983-12-01
Oxford Journals Open Access Collection
from 2002
ROAD: Directory of Open Access Scholarly Resources
from 1983
- MeSH
- Phylogeography MeSH
- Genetic Introgression * MeSH
- Histone-Lysine N-Methyltransferase genetics MeSH
- Infertility genetics MeSH
- Meiosis MeSH
- Mice genetics MeSH
- Reproductive Isolation * MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice genetics MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
The classical definition posits hybrid sterility as a phenomenon when two parental taxa each of which is fertile produce a hybrid that is sterile. The first hybrid sterility gene in vertebrates, Prdm9, coding for a histone methyltransferase, was identified in crosses between two laboratory mouse strains derived from Mus mus musculus and M. m. domesticus subspecies. The unique function of PRDM9 protein in the initiation of meiotic recombination led to the discovery of the basic molecular mechanism of hybrid sterility in laboratory crosses. However, the role of this protein as a component of reproductive barrier outside the laboratory model remained unclear. Here, we show that the Prdm9 allelic incompatibilities represent the primary cause of reduced fertility in intersubspecific hybrids between M. m. musculus and M. m. domesticus including 16 musculus and domesticus wild-derived strains. Disruption of fertility phenotypes correlated with the rate of failure of synapsis between homologous chromosomes in meiosis I and with early meiotic arrest. All phenotypes were restored to normal when the domesticus Prdm9dom2 allele was substituted with the Prdm9dom2H humanized variant. To conclude, our data show for the first time the male infertility of wild-derived musculus and domesticus subspecies F1 hybrids controlled by Prdm9 as the major hybrid sterility gene. The impairment of fertility surrogates, testes weight and sperm count, correlated with increasing difficulties of meiotic synapsis of homologous chromosomes and with meiotic arrest, which we suppose reflect the increasing asymmetry of PRDM9-dependent DNA double-strand breaks.
Department of Evolutionary Genetics Max Planck Institute for Evolutionary Biology Ploen Germany
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc21019638
- 003
- CZ-PrNML
- 005
- 20210830101225.0
- 007
- ta
- 008
- 210728s2020 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1093/molbev/msaa167 $2 doi
- 035 __
- $a (PubMed)32642764
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Mukaj, Amisa $u Department of Mouse Molecular Genetics, Institute of Molecular Genetics of the Czech Academy of Science, Vestec, Czech Republic
- 245 10
- $a Prdm9 Intersubspecific Interactions in Hybrid Male Sterility of House Mouse / $c A. Mukaj, J. Piálek, V. Fotopulosova, AP. Morgan, L. Odenthal-Hesse, ED. Parvanov, J. Forejt
- 520 9_
- $a The classical definition posits hybrid sterility as a phenomenon when two parental taxa each of which is fertile produce a hybrid that is sterile. The first hybrid sterility gene in vertebrates, Prdm9, coding for a histone methyltransferase, was identified in crosses between two laboratory mouse strains derived from Mus mus musculus and M. m. domesticus subspecies. The unique function of PRDM9 protein in the initiation of meiotic recombination led to the discovery of the basic molecular mechanism of hybrid sterility in laboratory crosses. However, the role of this protein as a component of reproductive barrier outside the laboratory model remained unclear. Here, we show that the Prdm9 allelic incompatibilities represent the primary cause of reduced fertility in intersubspecific hybrids between M. m. musculus and M. m. domesticus including 16 musculus and domesticus wild-derived strains. Disruption of fertility phenotypes correlated with the rate of failure of synapsis between homologous chromosomes in meiosis I and with early meiotic arrest. All phenotypes were restored to normal when the domesticus Prdm9dom2 allele was substituted with the Prdm9dom2H humanized variant. To conclude, our data show for the first time the male infertility of wild-derived musculus and domesticus subspecies F1 hybrids controlled by Prdm9 as the major hybrid sterility gene. The impairment of fertility surrogates, testes weight and sperm count, correlated with increasing difficulties of meiotic synapsis of homologous chromosomes and with meiotic arrest, which we suppose reflect the increasing asymmetry of PRDM9-dependent DNA double-strand breaks.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 12
- $a genová introgrese $7 D000079425
- 650 _2
- $a histonlysin-N-methyltransferasa $x genetika $7 D011495
- 650 _2
- $a infertilita $x genetika $7 D007246
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a meióza $7 D008540
- 650 _2
- $a myši $x genetika $7 D051379
- 650 _2
- $a fylogeografie $7 D058974
- 650 12
- $a reprodukční izolace $7 D060047
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Piálek, Jaroslav $u Research Facility Studenec, Institute of Vertebrate Biology of the Czech Academy of Sciences, Brno, Czech Republic
- 700 1_
- $a Fotopulosova, Vladana $u Department of Mouse Molecular Genetics, Institute of Molecular Genetics of the Czech Academy of Science, Vestec, Czech Republic
- 700 1_
- $a Morgan, Andrew Parker $u Department of Pediatrics, Duke University Hospital, Durham, NC
- 700 1_
- $a Odenthal-Hesse, Linda $u Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Ploen, Germany
- 700 1_
- $a Parvanov, Emil D $u Department of Mouse Molecular Genetics, Institute of Molecular Genetics of the Czech Academy of Science, Vestec, Czech Republic
- 700 1_
- $a Forejt, Jiri $u Department of Mouse Molecular Genetics, Institute of Molecular Genetics of the Czech Academy of Science, Vestec, Czech Republic
- 773 0_
- $w MED00006601 $t Molecular biology and evolution $x 1537-1719 $g Roč. 37, č. 12 (2020), s. 3423-3438
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/32642764 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20210728 $b ABA008
- 991 __
- $a 20210830101225 $b ABA008
- 999 __
- $a ok $b bmc $g 1690453 $s 1140084
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2020 $b 37 $c 12 $d 3423-3438 $e 20201216 $i 1537-1719 $m Molecular biology and evolution $n Mol Biol Evol $x MED00006601
- LZP __
- $a Pubmed-20210728