PMID- 28362806
OWN - NLM
STAT- MEDLINE
DCOM- 20170612
LR  - 20190202
IS  - 1553-7404 (Electronic)
IS  - 1553-7390 (Print)
IS  - 1553-7390 (Linking)
VI  - 13
IP  - 3
DP  - 2017 Mar
TI  - Evolved genetic and phenotypic differences due to mitochondrial-nuclear 
      interactions.
PG  - e1006517
LID - 10.1371/journal.pgen.1006517 [doi]
LID - e1006517
AB  - The oxidative phosphorylation (OxPhos) pathway is responsible for most aerobic 
      ATP production and is the only pathway with both nuclear and mitochondrial 
      encoded proteins. The importance of the interactions between these two genomes 
      has recently received more attention because of their potential evolutionary 
      effects and how they may affect human health and disease. In many different 
      organisms, healthy nuclear and mitochondrial genome hybrids between species or 
      among distant populations within a species affect fitness and OxPhos functions. 
      However, what is less understood is whether these interactions impact individuals 
      within a single natural population. The significance of this impact depends on 
      the strength of selection for mito-nuclear interactions. We examined whether 
      mito-nuclear interactions alter allele frequencies for ~11,000 nuclear SNPs 
      within a single, natural Fundulus heteroclitus population containing two 
      divergent mitochondrial haplotypes (mt-haplotypes). Between the two 
      mt-haplotypes, there are significant nuclear allele frequency differences for 349 
      SNPs with a p-value of 1% (236 with 10% FDR). Unlike the rest of the genome, 
      these 349 outlier SNPs form two groups associated with each mt-haplotype, with a 
      minority of individuals having mixed ancestry. We use this mixed ancestry in 
      combination with mt-haplotype as a polygenic factor to explain a significant 
      fraction of the individual OxPhos variation. These data suggest that mito-nuclear 
      interactions affect cardiac OxPhos function. The 349 outlier SNPs occur in genes 
      involved in regulating metabolic processes but are not directly associated with 
      the 79 nuclear OxPhos proteins. Therefore, we postulate that the evolution of 
      mito-nuclear interactions affects OxPhos function by acting upstream of OxPhos.
FAU - Baris, Tara Z
AU  - Baris TZ
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
FAU - Wagner, Dominique N
AU  - Wagner DN
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
FAU - Dayan, David I
AU  - Dayan DI
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
FAU - Du, Xiao
AU  - Du X
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
FAU - Blier, Pierre U
AU  - Blier PU
AD  - Dept de Biologie, Universite du Quebec a Rimouski, 300 Allee des Ursulines, 
      Rimouski, Quebec, Canada.
FAU - Pichaud, Nicolas
AU  - Pichaud N
AD  - Dept de Biologie, Universite du Quebec a Rimouski, 300 Allee des Ursulines, 
      Rimouski, Quebec, Canada.
FAU - Oleksiak, Marjorie F
AU  - Oleksiak MF
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
FAU - Crawford, Douglas L
AU  - Crawford DL
AD  - Marine Biology and Ecology, Rosenstiel School of Marine and Atmospheric Sciences, 
      University of Miami, Rickenbacker Causeway, Miami, FL, United States of America.
LA  - eng
SI  - Dryad/10.5061/dryad.nt461
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170331
PL  - United States
TA  - PLoS Genet
JT  - PLoS genetics
JID - 101239074
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (Fish Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Nuclear Proteins)
SB  - IM
CIN - PLoS Genet. 2017 Mar 31;13(3):e1006662. PMID: 28362804
MH  - Active Transport, Cell Nucleus/genetics
MH  - Animals
MH  - Cell Nucleus/*genetics/metabolism
MH  - DNA, Mitochondrial/genetics/metabolism
MH  - *Evolution, Molecular
MH  - Fish Proteins/genetics/metabolism
MH  - Fundulidae/*genetics/metabolism
MH  - Gene Frequency
MH  - Genetics, Population
MH  - Genotype
MH  - Haplotypes
MH  - Linkage Disequilibrium
MH  - Mitochondria/*genetics/metabolism
MH  - Mitochondrial Proteins/genetics/metabolism
MH  - Nuclear Proteins/genetics/metabolism
MH  - Oxidative Phosphorylation
MH  - Phenotype
MH  - Polymorphism, Single Nucleotide
PMC - PMC5375140
COIS- The authors have declared that no competing interests exist.
EDAT- 2017/04/01 06:00
MHDA- 2017/06/13 06:00
PMCR- 2017/03/31
CRDT- 2017/04/01 06:00
PHST- 2016/07/11 00:00 [received]
PHST- 2016/12/01 00:00 [accepted]
PHST- 2017/04/01 06:00 [entrez]
PHST- 2017/04/01 06:00 [pubmed]
PHST- 2017/06/13 06:00 [medline]
PHST- 2017/03/31 00:00 [pmc-release]
AID - PGENETICS-D-16-01525 [pii]
AID - 10.1371/journal.pgen.1006517 [doi]
PST - epublish
SO  - PLoS Genet. 2017 Mar 31;13(3):e1006517. doi: 10.1371/journal.pgen.1006517. 
      eCollection 2017 Mar.