521
While the majority of epigenetic marks are erased during gametogenesis and
embryo development, some parental marks may persist across multiple generations
(reviewed in Heard and Martienssen 2014; Skinner 2014; Hanson and Skinner
2016; Labbé et al. 2017). The genomic location of a mark, GC profile of the chromosomal region, mode of inheritance, and marker type may influence the likelihood
of a mark persisting from germline cell through embryogenesis (Hackett et al. 2013;
Tang et al. 2015; Szyf 2015; Blake and Watson 2016).
One stimulus that has been found to alter epigenetic state is toxin or toxicant
exposure. While exposure to toxins creates a xenobiotic response, as described in
the previous section, there are alterations to the epigenome that may also be
important. For example, when zebrafish are exposed to 2,3,7,8-tetrachlorodibenzop- dioxin (TCDD), genes in the AHR pathway are upregulated (Handley-Goldstone
et al. 2005; Carney et al. 2006). Aluru et al. (2015) found that TCDD exposure
caused changes in methylation state for two out of the three AHR pathway promoter
regions in concert with mRNA induction. There are many other examples of environmental toxins causing epigenetic alteration including changes in the methylation
state of the p53 and p16 genes in humans correlated with arsenic exposure (Chanda
et al. 2006), hypomethylation of the Igf2r, Peg3, and H19 genes in mice exposed to
the estrogen-like chemical diethylhexyl phthalate (Li et al. 2014), and altered global
methylation patterns in insects and humans exposed to insecticides (Collotta et al.
2013; Oppold and Müller 2017).
Only one study to date has analyzed the epigenetic state of any wild organism
with respect to the Deepwater Horizon (DWH) oil spill. Robertson et al. (2017)
found that there were five differentially methylated loci between oil-exposed and
non-oiled Spartina alterniflora, a salt marsh grass, but the genes associated with
these loci were not identified. Thirty-four other differentially methylated loci
between sampling sites (but not related to oil exposure) were also identified, so
follow-up work is needed to determine if the differential methylation was caused by
oil exposure. Other studies exist, however, that examine oil effects on fauna, environmental influence on epigenetic state, and transgenerational transmission of epigenetic marker. Oil-exposed fish embryos experience cardiac edema, yolk sac
edema, skeletal abnormalities, fin fold abnormalities, and decreased growth
(McEachern 2014; Xu et al. 2016b; Diamante et al. 2017). Transcriptional analysis
indicates that many of these characteristics are associated with differential gene
regulation during development (Xu et al. 2016b; Diamante et al. 2017). Exposure of
adult fish to oil indicates decreased swimming performance, possibly due to alterations in the cardiovascular system (Stieglitz et al. 2016). There are currently no
studies assessing whether phenotypic alterations are related to epigenetic modifications that could be passed on to future generations. There are also no known epigenetic marks that would function as biomarkers indicative of oil exposure though a
wealth of candidate genes are suggested by transcriptional analysis. Knecht et al.
(2017) did find global hypomethylation after benzo[a]pyrene (BaP) exposure, but
no specific locations were analyzed, and F 2 generations were not tested for altered
DNA methylation patterns.
30 Genetics and Oil: Transcriptomics, Epigenetics, and Population Genomics as Tools…
While the majority of epigenetic marks are erased during gametogenesis and
embryo development, some parental marks may persist across multiple generations
(reviewed in Heard and Martienssen 2014; Skinner 2014; Hanson and Skinner
2016; Labbé et al. 2017). The genomic location of a mark, GC profile of the chromosomal region, mode of inheritance, and marker type may influence the likelihood
of a mark persisting from germline cell through embryogenesis (Hackett et al. 2013;
Tang et al. 2015; Szyf 2015; Blake and Watson 2016).
One stimulus that has been found to alter epigenetic state is toxin or toxicant
exposure. While exposure to toxins creates a xenobiotic response, as described in
the previous section, there are alterations to the epigenome that may also be
important. For example, when zebrafish are exposed to 2,3,7,8-tetrachlorodibenzop- dioxin (TCDD), genes in the AHR pathway are upregulated (Handley-Goldstone
et al. 2005; Carney et al. 2006). Aluru et al. (2015) found that TCDD exposure
caused changes in methylation state for two out of the three AHR pathway promoter
regions in concert with mRNA induction. There are many other examples of environmental toxins causing epigenetic alteration including changes in the methylation
state of the p53 and p16 genes in humans correlated with arsenic exposure (Chanda
et al. 2006), hypomethylation of the Igf2r, Peg3, and H19 genes in mice exposed to
the estrogen-like chemical diethylhexyl phthalate (Li et al. 2014), and altered global
methylation patterns in insects and humans exposed to insecticides (Collotta et al.
2013; Oppold and Müller 2017).
Only one study to date has analyzed the epigenetic state of any wild organism
with respect to the Deepwater Horizon (DWH) oil spill. Robertson et al. (2017)
found that there were five differentially methylated loci between oil-exposed and
non-oiled Spartina alterniflora, a salt marsh grass, but the genes associated with
these loci were not identified. Thirty-four other differentially methylated loci
between sampling sites (but not related to oil exposure) were also identified, so
follow-up work is needed to determine if the differential methylation was caused by
oil exposure. Other studies exist, however, that examine oil effects on fauna, environmental influence on epigenetic state, and transgenerational transmission of epigenetic marker. Oil-exposed fish embryos experience cardiac edema, yolk sac
edema, skeletal abnormalities, fin fold abnormalities, and decreased growth
(McEachern 2014; Xu et al. 2016b; Diamante et al. 2017). Transcriptional analysis
indicates that many of these characteristics are associated with differential gene
regulation during development (Xu et al. 2016b; Diamante et al. 2017). Exposure of
adult fish to oil indicates decreased swimming performance, possibly due to alterations in the cardiovascular system (Stieglitz et al. 2016). There are currently no
studies assessing whether phenotypic alterations are related to epigenetic modifications that could be passed on to future generations. There are also no known epigenetic marks that would function as biomarkers indicative of oil exposure though a
wealth of candidate genes are suggested by transcriptional analysis. Knecht et al.
(2017) did find global hypomethylation after benzo[a]pyrene (BaP) exposure, but
no specific locations were analyzed, and F 2 generations were not tested for altered
DNA methylation patterns.
30 Genetics and Oil: Transcriptomics, Epigenetics, and Population Genomics as Tools…