No evidence for cumulative effects in a Dnmt3b hypomorph across multiple generations
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F13%3A00422963" target="_blank" >RIV/68378050:_____/13:00422963 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1007/s00335-013-9451-5" target="_blank" >http://dx.doi.org/10.1007/s00335-013-9451-5</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s00335-013-9451-5" target="_blank" >10.1007/s00335-013-9451-5</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
No evidence for cumulative effects in a Dnmt3b hypomorph across multiple generations
Popis výsledku v původním jazyce
Observations of inherited phenotypes that cannot be explained solely through genetic inheritance are increasing. Evidence points to transmission of non-DNA molecules in the gamete as mediators of the phenotypes. However, in most cases it is unclear whatthe molecules are, with DNA methylation, chromatin proteins, and small RNAs being the most prominent candidates. From a screen to generate novel mouse mutants of genes involved in epigenetic reprogramming, we produced a DNA methyltransferase 3b allele that is missing exon 13. Mice that are homozygous for the mutant allele have smaller stature and reduced viability, with particularly high levels of female post-natal death. Reduced DNA methylation was also detected at telocentric repeats and the X-linkedHprt gene. However, none of the abnormal phenotypes or DNA methylation changes worsened with multiple generations of homozygous mutant inbreeding. This suggests that in our model the abnormalities are reset each generation and the process
Název v anglickém jazyce
No evidence for cumulative effects in a Dnmt3b hypomorph across multiple generations
Popis výsledku anglicky
Observations of inherited phenotypes that cannot be explained solely through genetic inheritance are increasing. Evidence points to transmission of non-DNA molecules in the gamete as mediators of the phenotypes. However, in most cases it is unclear whatthe molecules are, with DNA methylation, chromatin proteins, and small RNAs being the most prominent candidates. From a screen to generate novel mouse mutants of genes involved in epigenetic reprogramming, we produced a DNA methyltransferase 3b allele that is missing exon 13. Mice that are homozygous for the mutant allele have smaller stature and reduced viability, with particularly high levels of female post-natal death. Reduced DNA methylation was also detected at telocentric repeats and the X-linkedHprt gene. However, none of the abnormal phenotypes or DNA methylation changes worsened with multiple generations of homozygous mutant inbreeding. This suggests that in our model the abnormalities are reset each generation and the process
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
EB - Genetika a molekulární biologie
OECD FORD obor
—
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2013
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Mammalian Genome
ISSN
0938-8990
e-ISSN
—
Svazek periodika
24
Číslo periodika v rámci svazku
5-6
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
12
Strana od-do
206-217
Kód UT WoS článku
000320659800005
EID výsledku v databázi Scopus
—