Search for: All records

Abstract Steranes preserved in sedimentary rocks serve as molecular fossils, which are thought to record the expansion of eukaryote life through the Neoproterozoic Era ( ~ 1000-541 Ma). Scientists hypothesize that ancient C₂₇steranes originated from cholesterol, the major sterol produced by living red algae and animals. Similarly, C₂₈and C₂₉steranes are thought to be derived from the sterols of prehistoric fungi, green algae, and other microbial eukaryotes. However, recent work on annelid worms–an advanced group of eumetazoan animals–shows that they are also capable of producing C₂₈and C₂₉sterols. In this paper, we explore the evolutionary history of the24-C sterol methyltransferase(smt) gene in animals, which is required to make C₂₈₊sterols. We find evidence that thesmtgene was vertically inherited through animals, suggesting early eumetazoans were capable of C₂₈₊sterol synthesis. Our molecular clock of the animalsmtgene demonstrates that its diversification coincides with the rise of C₂₈and C₂₉steranes in the Neoproterozoic. This study supports the hypothesis that early eumetazoans were capable of making C₂₈₊sterols and that many animal lineages independently abandoned its biosynthesis around the end-Neoproterozoic, coinciding with the rise of abundant eukaryotic prey. 

Social and behavioral epigenetics is the study of psychosocial factors that impact biology through an epigenetic mechanism. Epigenetic modifications influence the activity of genes without altering the underlying DNA sequence. DNA methylation is one type of epigenetic modification that has been widely studied and found to associate with a broad range of psychosocial stressors. This paper reviews the landmark studies and current innovations. An evolutionary context for epigenetic changes induced by psychosocial stress, and the possible heritability of such changes, is also presented. The involvement of social and behavioral scientists in this emerging field is essential to ensure that the nuances of the psychosocial environment are well understood and accurately modeled. 

Maternal stress has been linked to low birth weight in newborns. One potential pathway involves epigenetic changes at candidate genes that may mediate the effects of prenatal maternal stress on birth weight. This relationship has been documented in stress-related genes, such as NR3C1 . There is less literature exploring the effect of stress on growth-related genes. IGF1 and IGF2 have been implicated in fetal growth and development, though via different mechanisms as IGF2 is under imprinting control. In this study, we tested for associations between prenatal stress, methylation of IGF1 and IGF2 , and birth weight. A total of 24 mother–newborn dyads in the Democratic Republic of Congo were enrolled. Ethnographic interviews were conducted with mothers at delivery to gather culturally relevant war-related and chronic stressors. DNA methylation data were generated from maternal venous, cord blood and placental tissue samples. Multivariate regressions were used to test for associations between stress measures, DNA methylation and birth weight in each of the three tissue types. We found an association between IGF2 methylation in maternal blood and birth weight. Previous literature on the relationship between IGF2 methylation and birth weight has focused on methylation at known differentially methylated regions in cord blood or placental samples. Our findings indicate there may be links between the maternal epigenome and low birth weight that rely on mechanisms outside known imprinting pathways. It thus may be important to consider the effect of maternal exposures and epigenetic profiles on birth weight even in the setting of maternally imprinted genes such as IGF2 .