sanguineus-tropical lineage as a natural vector of Babesia vogeli and R. sanguineus-temperate lineage of SFGR. The acquisition of 190 CLE sequences allowed to evaluate co-phylogenetic associations between the tick and the symbiont. With this data, we observed a strong but incomplete co-cladogenesis between CLE strains and their Rhipicephalus tick lineages hosts. © FEMS 2020.Post-translational modifications provide suitable mechanisms for cellular adaptation to environmental changes. Lysine acetylation is one of these modifications and occurs with the addition of an acetyl group to Nε-amino chain of this residue, eliminating its positive charge. Recently, we found distinct acetylation profiles of procyclic and bloodstream forms of Trypanosoma brucei, the agent of African Trypanosomiasis. Interesting, glycolytic enzymes were more acetylated in the procyclic, which develops in insects and uses oxidative phosphorylation to obtain energy, compared with the bloodstream form, whose main source of energy is glycolysis. Here, we investigated whether acetylation regulates the T. brucei fructose 1,6-bisphosphate aldolase. We found that aldolase activity was reduced in procyclic parasites cultivated in the absence of glucose and partial recovered by in vitro deacetylation. Similarly, acetylation of protein extracts from procyclics cultivated in glucose-rich medium, caused a reduction in the aldolase activity. In addition, aldolase acetylation levels were higher in procyclics cultivated in the absence of glucose compared to those cultivated in the presence of glucose. To further confirm the role of acetylation, lysine residues near the catalytic site were substituted by glutamine in recombinant T. brucei aldolase. These replacements, especially K157, inhibited enzymatic activity, changed the electrostatic surface potential, decrease substrate binding and modify the catalytic pocket structure of the enzyme, as predicted by in silico analysis. Taken together, these data confirm the role of acetylation in regulating the activity of an enzyme from glycolytic pathway of T. brucei, expanding the factors responsible for regulating important pathways in this parasite. Copyright 2020 The Author(s).A homologue of the mitochondrial succinate/fumarate carrier from yeast (Sfc1p) has been found in the Arabidopsis genome, named AtSFC1. The AtSFC1 gene was expressed in Escherichia coli, and the gene product was purified and reconstituted in liposomes. Its transport properties and kinetic parameters demonstrated that AtSFC1 transports citrate, isocitrate and aconitate and, to a lesser extent, succinate and fumarate. This carrier catalyzes a fast counter-exchange transport as well as a low uniport of substrates, exhibits a higher transport affinity for tricarboxylates than dicarboxylates, and is inhibited by pyridoxal 5'-phosphate and other inhibitors of mitochondrial carriers to various degrees. Gene expression analysis indicated that the AtSFC1 transcript is mainly present in heterotrophic tissues and, fusion with a green-fluorescent protein localized AtSFC1 to the mitochondria. Furthermore, 35S-AtSFC1 antisense lines were generated and characterized at metabolic and physiological levels in different organs and at various developmental stages. Lower expression of AtSFC1 reduced seed germination and impaired radicle growth, a phenotype that was related with reduced respiration rate. These findings demonstrate that AtSFC1 might be involved in storage oil mobilization at early stages of seedling growth and in nitrogen assimilation in root tissue by catalyzing citrate/isocitrate or citrate/succinate exchanges. Copyright 2020 The Author(s).Previously we showed that contamination of SH-SY5Y neuroblastoma cells by Mycoplasma hyorhinis strains NDMh and MCLD leads to increased levels of calpastatin (the endogenous, specific inhibitor of the Ca2+-dependent protease calpain), resulting in inhibition of calpain activation. We have found that the increased calpastatin level is promoted by the lipoprotein fraction (MhLpp) of the mycoplasmal membrane. Here we present MhLpp-based novel synthetic lipopeptides that induce upregulation of calpastatin in SH-SY5Y neuroblastoma cells, leading to protection of the treated cells against Ca2+/amyloid-β-peptide toxicity. These lipopeptides present a new class of promising agents against calpain-induced cell toxicity. © FEMS 2020.BACKGROUND Little is known about life-course factors that explain why some individuals continue smoking despite having smoking-related diseases. PURPOSE We examined (a) the extent to which early-life adversities are associated with the risk of recalcitrant smoking, (b) psychosocial factors that mediate the association, and (c) gender differences in the associations. METHODS Data were from 4,932 respondents (53% women) who participated in the first and follow-up waves of the Midlife Development in the U.S. National Survey. Early-life adversities include low socioeconomic status (SES), abuse, and family instability.  https://www.selleckchem.com/products/rk-701.html  Potential mediators include education, financial strain, purpose in life, mood disorder, family problems/support, and marital status. We used sequential logistic regression models to estimate the effect of early-life adversities on the risk of each of the three stages on the path to recalcitrant smoking (ever-smoking, smoking-related illness, and recalcitrant smoking). RESULTS For women, low SES (odds ratio [OR] = 1.29; 1.06-1.55) and family instability (OR = 1.73; 1.14-2.62) are associated with an elevated risk of recalcitrant smoking. Education significantly reduces the effect of childhood SES, yet the effect of family instability remains significant even after accounting for life-course mediators. For men, the effect of low SES on recalcitrant smoking is robust (OR = 1.48; 1.10-2.00) even after controlling for potential mediators. There are noteworthy life-course factors that independently affect recalcitrant smoking for both genders, not living with a partner; for women, education; and for men, family problems. CONCLUSIONS The findings can help shape intervention programs that address the underlying factors of recalcitrant smoking. © Society of Behavioral Medicine 2020. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.