Congruence and responsiveness in the taxonomic compositions of Amazonian aquatic macroinvertebrate and fish assemblages

Hydrobiologia - Stream degradation in Amazonia is outpacing our ability to effectively monitor it for three key reasons: (1) Many changes are cumulative and occur gradually; (2) Scientists have...     

Biology and phenology of three leaf beetle species (Chrysomelidae) in a montane forest in southeast Brazil

The population phenology of the cassidines, Coptocycla arcuata and Omaspides trichroa, and the chrysomeline, Platyphora axillaris, was studied at Serra dos Órgãos National Park, State of Rio de Janeiro, southeast Brazil. Monthly surveys of larvae and adults were conducted between 2008 and 2011 at approximately 1000 m altitude on their respective host plants, Cordia polycephala (Boraginaceae), Ipomoea philomega (Convolvulaceae) and Solanum scuticum (Solanaceae). This is the first observation of larviparity and host record for Platyphora axillaris. Although having different life history traits, all species showed similar phenologies. They were abundant from October to March, months of high temperatures and intense rainfall, with two distinct reproductive peaks in the same season. Abundance dropped abruptly during the coldest and driest months, from May to August. Frequently none of these species were recorded during June and July. This phenological pattern is similar to other Chrysomelidae living in subtropical areas of Brazil. Temperature and rainfall appear to be the major factors influencing the fluctuation of these three species.     

Subacute calorie restriction and rapamycin discordantly alter mouse liver proteome homeostasis and reverse aging effects

Calorie restriction (CR) and rapamycin (RP) extend lifespan and improve health across model organisms. Both treatments inhibit mammalian target of rapamycin (mTOR) signaling, a conserved longevity pathway and a key regulator of protein homeostasis, yet their effects on proteome homeostasis are relatively unknown. To comprehensively study the effects of aging, CR, and RP on protein homeostasis, we performed the first simultaneous measurement of mRNA translation, protein turnover, and abundance in livers of young (3 month) and old (25 month) mice subjected to 10‐week RP or 40% CR. Protein abundance and turnover were measured in vivo using ²H₃–leucine heavy isotope labeling followed by LC‐MS/MS, and translation was assessed by polysome profiling. We observed 35–60% increased protein half‐lives after CR and 15% increased half‐lives after RP compared to age‐matched controls. Surprisingly, the effects of RP and CR on protein turnover and abundance differed greatly between canonical pathways, with opposite effects in mitochondrial (mt) dysfunction and eIF2 signaling pathways. CR most closely recapitulated the young phenotype in the top pathways. Polysome profiles indicated that CR reduced polysome loading while RP increased polysome loading in young and old mice, suggesting distinct mechanisms of reduced protein synthesis. CR and RP both attenuated protein oxidative damage. Our findings collectively suggest that CR and RP extend lifespan in part through the reduction of protein synthetic burden and damage and a concomitant increase in protein quality. However, these results challenge the notion that RP is a faithful CR mimetic and highlight mechanistic differences between the two interventions.     

Adaptive basal phosphorylation of eIF2α is responsible for resistance to cellular stress-induced cell death in Pten-null hepatocytes

The α-subunit of eukaryotic initiation factor 2 (eIF2α) is a key translation regulator that plays an important role in cellular stress responses. In the present study, we investigated how eIF2α phosphorylation can be regulated by a tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) and how such regulation is used by PTEN-deficient hepatocytes to adapt and cope with oxidative stress. We found that eIF2α was hyperphosphorylated when Pten was deleted, and this process was AKT dependent. Consistent with this finding, we found that the Pten-null cells developed resistance to oxidative glutamate and H(2)O(2)-induced cellular toxicity. We showed that the messenger level of CReP (constitutive repressor of eIF2α phosphorylation), a constitutive phosphatase of eIF2α, was downregulated in Pten-null hepatocytes, providing a possible mechanism through which PTEN/AKT pathway regulates eIF2α phosphorylation. Ectopic expression of CReP restored the sensitivity of the Pten mutant hepatocytes to oxidative stress, confirming the functional significance of the downregulated CReP and upregulated phospho-eIF2α in the resistance of Pten mutant hepatocytes to cellular stress. In summary, our study suggested a novel role of PTEN in regulating stress response through modulating the CReP/eIF2α pathway.