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Fernandes, G. W.

Publications and source records attributed to Fernandes, G. W..

4 recordsLinked to original sources

Plant secondary metabolite diversity reflects both phylogeny and ecological adaptation

A phylogenetic framework explaining plant secondary metabolite diversity is lacking, but metabolite classes could represent adaptations to habitat resource availability. We test the hypothesis that primary adaptive strategies (competitors, C; stress-tolerators, S; ruderals, R) are associated, respectively, with nitrogenous metabolites synthesized in persistent organs (alkaloids), nitrogen-lacking aromatic terpenes and phenolics, and nitrogenous compounds prevalent in reproductive tissues (cyanogenic glucosides and glucosinolates). A matrix was compiled of 1019 species for which secondary metabolite pathways and CSR strategies are known. Accounting for phylogenetic relatedness and native biomes, we found that most phytochemical pathways did not correlate with strategy axes, but certain key associations were evident. C-selection was positively associated with amino acid-derived phenylpropanoids (low phylogenetic relatedness; {lambda} <0.5) and pyrrolizidine alkaloids and galloyl derivatives (high {lambda}), and negatively with N-lacking linear monoterpenes (low {lambda}). Nitrogenous cyanogenic glucosides positively correlated with R-selection (low {lambda}). Terpenoids were widely distributed, but correlated positively with S- and negatively with R-selection (low {lambda}). Twenty-six correlations between phytochemicals and biomes (low {lambda}) were evident. Most secondary metabolite synthesis pathways are widespread, reflecting common roles and obligate defence, and strong phylogenetic effects are often evident. However, the character of phytochemical/adaptive strategy associations agrees with ecological theory and thus reflects adaptation.

ecology↗

NEONATAL THYROXINE ACTIVATION MODIFIES EPIGENETIC PROGRAMMING OF THE LIVER

In the neonatal liver, a peak of type 2 deiodinase (D2) activity accelerates local T3 production and the expression of thyroid hormone (TH)-responsive genes. Here we show that this acute increase in T3 signaling permanently modifies hepatic gene expression. Liver-specific Dio2 inactivation (Alb-D2KO) transiently increased H3K9me3 levels during post-natal days 1-5 (P1-P5) in discrete chromatin areas, and methylation of 1,508 DNA sites (H-sites) that remained in the adult mouse liver. These sites were associated with 1,551 areas of reduced chromatin accessibility (RCA; Atac-seq) within core promoters and 2,426 within intergenic regions, with reduction in the expression of 1,525 genes (RNA-seq). There was strong correlation between H-sites and RCA sites (r=0.85; p<0.0002), suggesting a cause-effect relationship. The analysis of chromosome conformation capture (Hi-C) data revealed a set of 57 repressed genes that have a promoter RCA in close contact with an intergenic RCA ~300 Kbp apart, including Foxa2 that plays an important role during development. Thus, the post-natal surge in hepatic D2 activity and TH-signaling prevents discrete DNA methylation and modifies the transcriptome of the adult mouse. This explains how the systemic T3 hormone acts locally during development to define future chromatin accessibility and expression of critically relevant hepatic genes.

physiology↗

The transcriptional repressor Zfp125 modifies hepatic energy metabolism in response to fasting and insulin resistance

Zfp125 is a transcriptional repressor that inhibits hepatic VLDL secretion. Here we show that mice with liver-specific Zfp125 knockdown exhibited lower respiratory quotient, reduced glycemia and pyruvate-stimulated liver glucose output, and higher levels of {beta}-hydroxyl-butyrate. Microarray and ChIP-seq studies identified Zfp125 peaks in the promoter of 135 metabolically relevant genes, including genes involved in fatty acid oxidation and ketogenesis, e.g. Ppara, Cpt1a, Bdh1 and Hmgcs2. Repression by Zfp125 involved recruitment of the corepressors Kap1 and the histone methyl transferase Setdb1, increasing the levels of H3K9me3, a heterochromatin marker of gene silencing. The resulting increase in acetyl-CoA levels accelerated gluconeogenesis through allosteric activation of pyruvate carboxylase. Zfp125 knockdown in isolated mouse hepatocytes amplified the induction of ketogenesis by glucagon or insulin resistance, whereas the expression of key gluconeogenic genes Pck1 and G6pc was amplified by Zfp125. These findings place Zfp125 at the center of fuel dysregulation of type 2 diabetes.

physiology↗

The mistletoe Struthanthus flexicaulis reduces dominance and increases diversity of plants in campo rupestre

The interaction between hemiparasites and their host plants is an important structuring mechanism for plant communities. The mistletoe Struthanthus flexicaulis (Loranthaceae) is widely distributed in the campo rupestre ecosystem and likely has an important role in structuring the communities of which its hosts are part. The main goals of this study were to investigate the effects of parasitism by S. flexicaulis on host plants in a degraded area of campo rupestre and to determine how parasitism affects characteristics of the structure of this plant community over time. We found that parasitized plants had smaller crowns and branch growth, and suffered lower mortality compared to non-parasitized plants. Parasitism by S. flexicaulis decreased dominance and increased the diversity and evenness of plants in the community over time. Parasitism leads to competition with the host for water and nutrients, which may decrease the performance of the host and, consequently, leading to host death. The high mortality of the most abundant plant species led to a restructured woody plant community. These results reinforce the importance of parasitic plants as key species for maintaining species diversity in plant communities.

ecology↗