Genomic imprinting analyses identify maternal effects as a cause of phenotypic variability in type 1 diabetes and rheumatoid arthritis
(2020) In Scientific Reports 10(1).- Abstract
Imprinted genes, giving rise to parent-of-origin effects (POEs), have been hypothesised to affect type 1 diabetes (T1D) and rheumatoid arthritis (RA). However, maternal effects may also play a role. By using a mixed model that is able to simultaneously consider all kinds of POEs, the importance of POEs for the development of T1D and RA was investigated in a variance components analysis. The analysis was based on Swedish population-scale pedigree data. With P = 0.18 (T1D) and P = 0.26 (RA) imprinting variances were not significant. Explaining up to 19.00% (± 2.00%) and 15.00% (± 6.00%) of the phenotypic variance, the maternal environmental variance was significant for T1D (P = 1.60 × 10−24) and for RA (P = 0.02). For the first... (More)
Imprinted genes, giving rise to parent-of-origin effects (POEs), have been hypothesised to affect type 1 diabetes (T1D) and rheumatoid arthritis (RA). However, maternal effects may also play a role. By using a mixed model that is able to simultaneously consider all kinds of POEs, the importance of POEs for the development of T1D and RA was investigated in a variance components analysis. The analysis was based on Swedish population-scale pedigree data. With P = 0.18 (T1D) and P = 0.26 (RA) imprinting variances were not significant. Explaining up to 19.00% (± 2.00%) and 15.00% (± 6.00%) of the phenotypic variance, the maternal environmental variance was significant for T1D (P = 1.60 × 10−24) and for RA (P = 0.02). For the first time, the existence of maternal genetic effects on RA was indicated, contributing up to 16.00% (± 3.00%) of the total variance. Environmental factors such as the social economic index, the number of offspring, birth year as well as their interactions with sex showed large effects.
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- author
- Blunk, Inga LU ; Thomsen, Hauke LU ; Reinsch, Norbert ; Mayer, Manfred ; Försti, Asta LU ; Sundquist, Jan LU ; Sundquist, Kristina LU and Hemminki, Kari LU
- organization
- publishing date
- 2020-07-14
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 10
- issue
- 1
- article number
- 11562
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:32665606
- scopus:85087965449
- ISSN
- 2045-2322
- DOI
- 10.1038/s41598-020-68212-x
- language
- English
- LU publication?
- yes
- id
- 4d928c3f-603a-433b-bad5-897b7612fbc4
- date added to LUP
- 2020-07-25 08:29:20
- date last changed
- 2024-09-05 02:14:54
@article{4d928c3f-603a-433b-bad5-897b7612fbc4, abstract = {{<p>Imprinted genes, giving rise to parent-of-origin effects (POEs), have been hypothesised to affect type 1 diabetes (T1D) and rheumatoid arthritis (RA). However, maternal effects may also play a role. By using a mixed model that is able to simultaneously consider all kinds of POEs, the importance of POEs for the development of T1D and RA was investigated in a variance components analysis. The analysis was based on Swedish population-scale pedigree data. With P = 0.18 (T1D) and P = 0.26 (RA) imprinting variances were not significant. Explaining up to 19.00% (± 2.00%) and 15.00% (± 6.00%) of the phenotypic variance, the maternal environmental variance was significant for T1D (P = 1.60 × 10<sup>−24</sup>) and for RA (P = 0.02). For the first time, the existence of maternal genetic effects on RA was indicated, contributing up to 16.00% (± 3.00%) of the total variance. Environmental factors such as the social economic index, the number of offspring, birth year as well as their interactions with sex showed large effects.</p>}}, author = {{Blunk, Inga and Thomsen, Hauke and Reinsch, Norbert and Mayer, Manfred and Försti, Asta and Sundquist, Jan and Sundquist, Kristina and Hemminki, Kari}}, issn = {{2045-2322}}, language = {{eng}}, month = {{07}}, number = {{1}}, publisher = {{Nature Publishing Group}}, series = {{Scientific Reports}}, title = {{Genomic imprinting analyses identify maternal effects as a cause of phenotypic variability in type 1 diabetes and rheumatoid arthritis}}, url = {{http://dx.doi.org/10.1038/s41598-020-68212-x}}, doi = {{10.1038/s41598-020-68212-x}}, volume = {{10}}, year = {{2020}}, }