We draw two major conclusions from our work. Firstly, by observing changes in heteroplasmy levels from mothers to oocytes and offspring, we can confirm that a mitochondrial genetic bottleneck, or bottleneck effect, exists in chinook salmon during early developmental stages. Thus, salmon appear congruent with an array of other taxonomic groups 
. Secondly, the similarity between NeOog
(88.3) and NeEmb
(80.3), as found here, indicates that the main mitochondrial genetic bottleneck occurs during oogenesis in salmon. Although we found NeOog
to be slightly higher than NeEmb
, this difference was not significantly different. As estimates of Ne
are directly correlated to measurement error, the greater value of Ne
for oogenesis may be due to a larger measurement error for oocytes (1.67%), compared to that for F1 offspring (1.18%). Alternatively, random sample choice could have led to the chance selection of oocyte samples with less variation in heteroplasmy measurements, leading to a higher estimate of NeOog
. A third possibility is that a further, non-significant, reduction in effective mtDNA copy number occurs during embryogenesis.
Our results tie in with those of earlier studies which proposed that segregation is likely to occur prior to the differentiation of the primary oocyte population during oogenesis in mouse 
. Possible mechanisms underlying heteroplasmy shifts in oocytes have been proposed and include relaxed replication of mtDNA, and random partitioning of mitochondria 
, which typically depend on vast cell proliferation and mtDNA replication, two processes that can be observed during germ line development 
Previous studies suggest that the size of the intergenerational mtDNA bottleneck is unexpectedly similar across a wide range of different taxa, spanning invertebrates to vertebrates, supporting the idea of a conserved mechanism across taxa 
. Our estimates of NeOog
for chinook salmon are in concordance with those of mammals 
and crickets 
, and within the same order of magnitude as fruit flies 
; despite the 10,000-fold higher mtDNA content of chinook salmon versus mammalian oocytes, and differences in cleavage patterns (rotational holoblastic in mammals vs. discoidal meroblastic in teleosts) 
. Further, the mechanism in salmon demonstrates striking similarities to those found in mice, according to two studies, in that segregation of heteroplasmy can be accounted for during oogenesis 
. Thus, our findings strongly indicate that mechanisms of mitochondrial inheritance may be conserved and of a comparable nature among divergent taxa.
The intergenerational transmission of mitochondrial heteroplasmy has many important biological implications. First, the transmission of heteroplasmy has direct impact on the inheritance of mitochondrial diseases 
- most of which are observed in a heteroplasmic form and expressed when the deleterious allele exceeds a certain threshold 
. Second, heteroplasmy may also create some ambiguity in phylogenetic and network interpretations of population data of mtDNA 
. Third, heteroplasmy will create the possibility for intermolecular recombination 
, which might further affect the evolution of the mtDNA molecule and thus evolutionary analysis based on this molecule 
, but also may enable the molecule to escape the mutational meltdown expected if it were solely inherited in a clonal fashion 
. On the other hand, the inclusion of knowledge of the frequency and stability of mtDNA heteroplasmy would increase the level of molecular information available from, and may improve the resolution of, mtDNA focused analyses in evolutionary, forensic and medical science 
For example, heteroplasmic states that are stably inherited for significant periods may provide useful additional information for defining haplotypes, and resolving further the relationships among individuals at a population level 
. Thus far such an approach has been used rarely 
, but there is potential for this to increase if we better understand the mtDNA bottleneck and can therefore predict how long such mutations might persist. A simple mutation drift model predicts that a mtDNA bottleneck of Ne
100 leads to a predicted time to fixation for a neutral, mitochondrial, heteroplasmic variant of approximately 200 generations 
; long enough to impact significantly on population genetic interpretations.
In this study, we have demonstrated the existence of a mtDNA bottleneck in a teleost, the first non-mammalian vertebrate to be examined. Despite fundamental differences in physiology and developmental cleavage pattern, the number of segregating units between generations appears remarkably similar to that found in other species, including mouse. This finding suggests the mitochondrial bottleneck might be conserved among divergent taxa. However, across the animal kingdom, our knowledge of the mechanisms underlying mtDNA inheritance is far from complete, and many more studies of this nature are required to further understand this important evolutionary process, and thus capture the full extent of the additional value that an understanding of heteroplasmy may bring to the life sciences.