Plant communities of large portions of the southwestern United States have changed from grassland to desert shrubland. Previous studies have demonstrated that soil nutrient resources become spatially more heterogeneous and are redistributed into islands of fertility with the shift in vegetation. The research presented here addressed the question of whether soil resources become more temporally heterogeneous as well as more spatially heterogeneous when grassland undergoes desertification to form shrubland. Within adjacent grassland and creosotebush sites, soil profiles were described at three soil pits, and samples were collected for description of nutrient resources within the profile. Relative abundance of plant cover and bare soil was determined within each site using line transects. Surface samples (0–20 cm depth) of bare soil and soil beneath the canopies of grasses and creosotebush were collected 17 times during 1992–1994. Soil samples were analyzed for moisture, extractable ammonium and nitrate, nitrogen mineralization potential, microbial biomass carbon, total organic carbon, microbial respiration, dehydrogenase activity, the ratio of microbial C to total organic C (Cmic/Corg), and the ratio of microbial respiration to biomass carbon (metabolic quotient). The major differences in the structure of soils between sites were the apparent loss of 3–5 cm depth of sandy surface soil at the creosotebush site and an associated increase in calcium carbonate content at a more shallow depth. Soils under plants at both sites had greater total and available nutrient resources, with higher concentrations under creosotebush than under grasses. Greatest temporal variation in available soil resources was observed in soils under creosotebush. When expressed on the basis of area, available soil resources were higher in the grassland than in the creosotebush shrubland, primarily due to the difference in plant cover (45% in grassland, 8% in creosotebush shrubland).

Several genome-wide screens have indicated the presence of an autism susceptibility locus within the distal long arm of chromosome 7 (7q). Mapping at 7q22 within this region is the candidate gene reelin (RELN). RELN encodes a signaling protein that plays a pivotal role in the migration of several neuronal cell types and in the development of neural connections. Given these neurodevelopmental functions, recent reports that RELN influences genetic risk for autism are of significant interest. The total data set consists of 218 Caucasian families collected by our group, 85 Caucasian families collected by AGRE, and 68 Caucasian families collected at Tufts University were tested for genetic association of RELN variants to autism. Markers included five single-nucleotide polymorphisms (SNPs) and a repeat in the 5 0 -untranslated region (5 0 -UTR). Tests for association in Duke and AGRE families were also performed on four additional SNPs in the genes PSMC2 and ORC5L, which flank RELN. Familybased association analyses (PDT, Geno-PDT, and FBAT) were used to test for association of single-locus markers and multilocus haplotypes with autism. The most significant association identified from this combined data set was for the 5 0 -UTR repeat (PDT P-value ¼ 0.002). These analyses show the potential of RELN as an important contributor to genetic risk in autism.

BackgroundCadmium (Cd) is a ubiquitous and environmentally persistent toxic metal that has been implicated in neurotoxicity, carcinogenesis and obesity and essential metals including zinc (Zn) and iron (Fe) may alter these outcomes. However mechanisms underlying these relationships remain limited.MethodsWe examined whether maternal Cd levels during early pregnancy were associated with offspring DNA methylation at regulatory sequences of genomically imprinted genes and weight at birth, and whether Fe and Zn altered these associations. Cd, Fe and Zn were measured in maternal blood of 319 women ≤12 weeks gestation. Offspring umbilical cord blood leukocyte DNA methylation at regulatory differentially methylated regions (DMRs) of 8 imprinted genes was measured using bisulfite pyrosequencing. Regression models were used to examine the relationships among Cd, Fe, Zn, and DMR methylation and birth weight.ResultsElevated maternal blood Cd levels were associated with lower birth weight (p = 0.03). Higher maternal blood Cd levels were also associated with lower offspring methylation at the PEG3 DMR in females (β = 0.55, se = 0.17, p = 0.05), and at the MEG3 DMR in males (β = 0.72, se = 0.3, p = 0.08), however the latter association was not statistically significant. Associations between Cd and PEG3 and PLAGL1 DNA methylation were stronger in infants born to women with low concentrations of Fe (p < 0.05).ConclusionsOur data suggest the association between pre-natal Cd and offspring DNA methylation at regulatory sequences of imprinted genes may be sex- and gene-specific. Essential metals such as Zn may mitigate DNA methylation response to Cd exposure. Larger studies are required.

Humans are exposed to low-dose ionizing radiation (LDIR) from a number of environmental and medical sources. In addition to inducing genetic mutations, there is concern that LDIR may also alter the epigenome. Such heritable effects early in life can either be positively adaptive or result in the enhanced formation of diseases, including cancer, diabetes, and obesity. Herein, we show that LDIR significantly increased DNA methylation at the viable yellow agouti (A(vy)) locus in a sex-specific manner (P=0.004). Average DNA methylation was significantly increased in male offspring exposed to doses between 0.7 and 7.6 cGy, with maximum effects at 1.4 and 3.0 cGy (P<0.01). Offspring coat color was concomitantly shifted toward pseudoagouti (P<0.01). Maternal dietary antioxidant supplementation mitigated both the DNA methylation changes and coat color shift in the irradiated offspring. Thus, LDIR exposure during gestation elicits epigenetic alterations that lead to positive adaptive phenotypic changes that are negated with antioxidants, indicating they are mediated in part by oxidative stress. These findings provide evidence that in the isogenic A(vy) mouse model, epigenetic alterations resulting from LDIR play a role in radiation hormesis, bringing into question the assumption that every dose of radiation is harmful.

Imprinted genes form a special subset of the genome, exhibiting monoallelic expression in a parent-of-origin–dependent fashion. This monoallelic expression is controlled by parental-specific epigenetic marks, which are established in gametogenesis and early embryonic development and are persistent in all somatic cells throughout life. We define this specific set of cis-acting epigenetic regulatory elements as the imprintome, a distinct and specially tasked subset of the epigenome. Imprintome elements contain DNA methylation and histone modifications that regulate monoallelic expression by affecting promoter accessibility, chromatin structure, and chromatin configuration. Understanding their regulation is critical because a significant proportion of human imprinted genes are implicated in complex diseases. Significant species variation in the repertoire of imprinted genes and their epigenetic regulation, however, will not allow model organisms solely to be used for this crucial purpose. Ultimately, only the human will suffice to accurately define the human imprintome.

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology. Abstract.Plant communities of large portions of the southwestern United States have changed from grassland to desert shrubland. Previous studies have demonstrated that soil nutrient resources become spatially more heterogeneous and are redistributed into islands of fertility with the shift in vegetation. The research presented here addressed the question of whether soil resources become more temporally heterogeneous as well as more spatially heterogeneous when grassland undergoes desertification to form shrubland. Within adjacent grassland and creosotebush sites, soil profiles were described at three soil pits, and samples were collected for description of nutrient resources within the profile. Relative abundance of plant cover and bare soil was determined within each site using line transects. Surface samples (0-20 cm depth) of bare soil and soil beneath the canopies of grasses and creosotebush were collected 17 times during 1992-1994. Soil samples were analyzed for moisture, extractable ammonium and nitrate, nitrogen mineralization potential, microbial biomass carbon, total organic carbon, microbial respiration, dehydrogenase activity, the ratio of microbial C to total organic C (Cmic/Corg), and the ratio of microbial respiration to biomass carbon (metabolic quotient). The major differences in the structure of soils between sites were the apparent loss of 3-5 cm depth of sandy surface soil at the creosotebush site and an associated increase in calcium carbonate content at a more shallow depth. Soils under plants at both sites had greater total and available nutrient resources, with higher concentrations under creosotebush than under grasses. Greatest temporal variation in available soil resources was observed in soils under creosotebush. When expressed on the basis of area, available soil resources were higher in the grassland than in the creosotebush shrubland, primarily due to the difference in plant cover (45% in grassland, 8% in creosotebush shrubland).

Background:Lead exposure during early development causes neurodevelopmental disorders by unknown mechanisms. Epidemiologic studies have focused recently on determining associations between lead exposure and global DNA methylation; however, such approaches preclude the identification of loci that may alter human disease risk.Objectives:The objective of this study was to determine whether maternal, postnatal, and early childhood lead exposure can alter the differentially methylated regions (DMRs) that control the monoallelic expression of imprinted genes involved in metabolism, growth, and development.Methods:Questionnaire data and serial blood lead levels were obtained from 105 participants (64 females, 41 males) of the Cincinnati Lead Study from birth to 78 months. When participants were adults, we used Sequenom EpiTYPER assays to test peripheral blood DNA to quantify CpG methylation in peripheral blood leukocytes at DMRs of 22 human imprinted genes. Statistical analyses were conducted using linear regression.Results:Mean blood lead concentration from birth to 78 months was associated with a significant decrease in PEG3 DMR methylation (β = –0.0014; 95% CI: –0.0023, –0.0005, p = 0.002), stronger in males (β = –0.0024; 95% CI: –0.0038, –0.0009, p = 0.003) than in females (β = –0.0009; 95% CI: –0.0020, 0.0003, p = 0.1). Elevated mean childhood blood lead concentration was also associated with a significant decrease in IGF2/H19 (β = –0.0013; 95% CI: –0.0023, –0.0003, p = 0.01) DMR methylation, but primarily in females, (β = –0.0017; 95% CI: –0.0029, –0.0006, p = 0.005) rather than in males, (β = –0.0004; 95% CI: –0.0023, 0.0015, p = 0.7). Elevated blood lead concentration during the neonatal period was associated with higher PLAGL1/HYMAI DMR methylation regardless of sex (β = 0.0075; 95% CI: 0.0018, 0.0132, p = 0.01). The magnitude of associations between cumulative lead exposure and CpG methylation remained unaltered from 30 to 78 months.Conclusions:Our findings provide evidence that early childhood lead exposure results in sex-dependent and gene-specific DNA methylation differences in the DMRs of PEG3, IGF2/H19, and PLAGL1/HYMAI in adulthood.Citation:Li Y, Xie C, Murphy SK, Skaar D, Nye M, Vidal AC, Cecil KM, Dietrich KN, Puga A, Jirtle RL, Hoyo C. 2016. Lead exposure during early human development and DNA methylation of imprinted gene regulatory elements in adulthood. Environ Health Perspect 124:666–673; http://dx.doi.org/10.1289/ehp.1408577

There are several kinases in Saccharomyces cerevisiae that phosphorylate the CTD of RNA polymerase II, but specific and distinct functions of the phospho-CTDs generated by the different kinases are not well understood. A genetic screen for suppressors of loss of yeast CTD kinase I (CTDK-I) function (by deletion of the catalytic subunit gene CTK1) identified PTI1, a potential 3' cleavage/polyadenylation factor. Genetic and physical interactions connect Pti1p to components of CF IA and CF II/CPF, and mutations of PTI1 or CTK1 affect 3' cleavage site choice and transcript abundance of particular genes. Therefore, one important function of the CTDK-I-generated phospho-CTD appears to be the coupling of transcription to 3' processing of pre-mRNAs by a Pti1p-containing complex.