The NAC transcription factor ATAF2 suppresses its own transcription via self-promoter binding. ATAF2 genetically interacts with the circadian regulator CCA1 and phytochrome A to modulate seedling photomorphogenesis in Arabidopsis thaliana. ATAF2 (ANAC081) is a NAC (NAM, ATAF and CUC) transcription factor (TF) that participates in the regulation of disease resistance, stress tolerance and hormone metabolism in Arabidopsis thaliana. We previously reported that ATAF2 promotes Arabidopsis hypocotyl growth in a light-dependent manner via transcriptionally suppressing the brassinosteroid (BR)-inactivating cytochrome P450 genes BAS1 (CYP734A1, formerly CYP72B1) and SOB7 (CYP72C1). Assays using low light intensities suggest that the photoreceptor phytochrome A (PHYA) may play a more critical role in ATAF2-regulated photomorphogenesis than phytochrome B (PHYB) and cryptochrome 1 (CRY1). In addition, ATAF2 is also regulated by the circadian clock. The core circadian TF CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) physically i circadian-clock-photomorphogenesis-BR integration node involving ATAF2, CCA1 and PHYA.Acquired immunodeficiency syndrome (AIDS) caused by human immunodeficiency virus (HIV) is a major global public health problem. The aim of this study is to determine the prevalence of HIV-1 infection in four municipalities of Pará State (Marabá, Parauapebas, Curionópolis, and Canaã dos Carajás), in northern, Brazil. The municipalities are located in the Carajás Complex iron mining area. The employment opportunities result in extensive migratory flow of people. A total of 4771 serum samples were obtained from 2005 to 2014 and were sent to Evandro Chagas Institute, Belém-Pará, where they were tested by enzyme-linked immunosorbent assay, with reactive samples confirmed by Western blot analysis. The samples were from individuals from 23 Brazilian states and the Federal District, mainly Maranhão (39.53%) and other municipalities of Pará (34.25%). The total positivity rate was 0.48% (23/4771). The rate was 0.47% (14/2975) in males and 0.50% (9/1796) in females. Of these, 0.33% (14/4275) were from asymptomatic individuals whose serum were collected during the serological survey, 1.81% (9/497) were from cases featuring clinical symptoms including fever/diarrhea/jaundice, which were included in febrile, diarrheal, and icteric syndromes analyzed during the study. The findings indicated the presence of HIV-1 infection in the general population studied. The majority of cases (60.9%, 14 of 23 positive cases) were asymptomatic.Root hairs (RHs) are single-celled elongated epidermal cells and play a vital role in nutrient absorption, particularly for immobile minerals like phosphorus (P). As an adaptive response to P deficiency, an increase in RH length enhances root-soil contact and absorptive area for P absorption. Genetic variations have been reported for RH length and its response to P deficiency in plants. However, only a few association studies have been conducted to identify genes and genetic loci associated with RH length. Here, we screened desi chickpea accessions for RH length and its plasticity under P deficiency. Further, the genome-wide association study (GWAS) was conducted to identify the genetic loci associated with RH length in P deficient and sufficient conditions. Although high variability was observed in terms of RH length in diverse genotypes, majority of the accessions showed typical response of increase in RH length in low P. Genome-wide association mapping identified many SNPs with significant associations with RH length in P-sufficient and P-deficient conditions. A few candidate genes for RH length in P deficient (SIZ1-like and HAD superfamily protein) and sufficient (RSL2-like and SMAP1-like) conditions were identified which have known roles in RH development and P deficiency response or both. Torin 1 Highly associated loci and candidate genes identified in this study would be useful for genomic-assisted breeding to develop P-efficient chickpea.SUMOylation is a post-translational modification (PTM) whereby members of the Small Ubiquitin-like MOdifier (SUMO) family of proteins are conjugated to lysine residues in target proteins. SUMOylation has been implicated in a wide range of physiological and pathological processes, and much attention has been given to its role in neurodegenerative conditions. Due to its reported role in neuroprotection, pharmacological modulation of SUMOylation represents an attractive potential therapeutic strategy in a number of different brain disorders. However, very few compounds that target the SUMOylation pathway have been identified. Guanosine is an endogenous nucleoside with important neuromodulatory and neuroprotective effects. Experimental evidence has shown that guanosine can modulate different intracellular pathways, including PTMs. In the present study we examined whether guanosine alters global protein SUMOylation. Primary cortical neurons and astrocytes were treated with guanosine at 1, 10, 100, 300, or 500 μM at four time points, 1, 6, 24, or 48 h. We show that guanosine increases global SUMO2/3-ylation in neurons and astrocytes at 1 h at concentrations above 10 μM. The molecular mechanisms involved in this effect were evaluated in neurons. The guanosine-induced increase in global SUMO2/3-ylation was still observed in the presence of dipyridamole, which prevents guanosine internalization, demonstrating an extracellular guanosine-induced effect. Furthermore, the A1 adenosine receptor antagonist DPCPX abolished the guanosine-induced increase in SUMO2/3-ylation. The A2A adenosine receptor antagonist ZM241385 increased SUMOylation per se, but did not alter guanosine-induced SUMOylation, suggesting that guanosine may modulate SUMO2/3-ylation through an A1-A2A receptor interaction. Taken together, this is the first report to show guanosine as a SUMO2/3-ylation enhancer in astrocytes and neurons.Diets that have effects on health problems can vary in their composition. Whilst following a regular diet (RD) a person typically consumes about 30% of calories from fat. Ketogenic diet (KD) is a form of diet whereby a person consumes as much as 90% of calories from fat. KD has been trialed as a treatment for neurological diseases and obesity. Parkinson’s disease (PD) is a neurologic disease that impacts the quality of voice. Voice Handicap Index (VHI) is a test that gives information to clinical and physiological assessment about voice. We assessed the impact of KD and RD on voice quality (VQ). Seventy-four patients with PD who reported a voice disorder related to their disease were randomly assigned to the KD or RD groups. We investigated the VHI change of subjects before and 3 months after diet. Sixty-eight PD patients completed the study. Baseline VHI values did not differ significantly between groups. All mean VHI parameters improved in KD group (p˂ 0.001). Currently there are different therapies that address speech and voice disorders in patients with PD.