COP1 dynamics integrate conflicting seasonal light and thermal cues in the control of elongation.

As the summer approaches, plants experience enhanced light inputs and warm temperatures, two environmental cues with an opposite morphogenic impact. Key components of this response are PHYTOCHROME B (phyB), EARLY FLOWERING 3 (ELF3), and CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1). Here, we used single and double mutant/overexpression lines to fit a mathematical model incorporating known interactions of these regulators.

Regulation of COP1 Function by Brassinosteroid Signaling.

Small increases in temperature result in enhanced elongation of the hypocotyl and petioles and hyponastic growth, in an adaptive response directed to the cooling of the leaves and to protect the shoot meristem from the warm soil. This response, collectively termed as thermomorphogenesis, relies on the faster reversion of phyB Pfr at warmer temperatures, which leads to enhanced activity of the basic-helix-loop-helix PHYTOCHROME INTERACTING FACTOR 4 (PIF4). PIF4 acts as a molecular hub integrating light and temperature cues with endogenous hormonal signaling, and drives thermoresponsive growth by directly activating auxin synthesis and signaling genes.

Successful Establishment of Plasmids R1 and pMV158 in a New Host Requires the Relief of the Transcriptional Repression of Their Essential Genes.

Although differing in size, encoded traits, host range, and replication mechanism, both narrow-host-range theta-type conjugative enterobacterial plasmid R1 and promiscuous rolling-circle-type mobilizable streptococcal plasmid pMV158 encode a transcriptional repressor protein, namely CopB in R1 and CopG in pMV158, involved in replication control. The gene encoding CopB or CopG is cotranscribed with a downstream gene that encodes the replication initiator Rep protein of the corresponding plasmid. However, whereas CopG is an auto-repressor that inhibits transcription of the entire operon, CopB is expressed constitutively and represses a second, downstream promoter that directs transcription of .

[Home parenteral nutrition: a consensus document of experts from Andalucia and Extremadura].

Home parenteral nutrition (HPN) is a technique that has allowed the survival in the community of those patients with serious diseases resulting in an intestinal failure that made their nutrition impossible by other methods. It is indicated if there is a documented intestinal failure (understood by the reduction of the intestinal function to the minimum to the point that intravenous supplementation is required to maintain health and/or growth) with impossibility for oral or enteral exclusive nutrition, provided that there is the possibility of managing the patient at home and that there is no short-term survival expectancy. It requires taking into account the patient's quality of life, family environment and the capacity of the patient and/or their caregivers to be trained for HPN therapy.

[Spanish home enteral nutrition registry of the year 2014 and 2015 from the NADYA-SENPE Group].

Objective: To present the results of the Spanish home enteral nutrition (HEN) registry of the NADYA-SENPE group for the years 2014 and 2015. Methods: From January 1st 2014 to December 31st 2015 the HEN registry was recorded and afterwards a further descriptive and analytical analysis was done. Results: In 2014, 3749 patients were recorded, and 4202 in 2015; prevalence was 80.

[Anthropometric measures of central abdominal fat and discriminant capacity for metabolic syndrome in a Spanish population].

Introduction: The metabolic syndrome (MS) carries an increased risk of cardiovascular disease and diabetes mellitus. Insulin resistance is probably the mechanism underlying the changes detected in lipid and carbohydrate metabolism in these patients, who have, as a common anthropometric feature, a predominantly increased abdominal fat distribution.

Patients And Methods: A total of 3316 patients were studied, of whom 63.

[Association of FTO gene polymorphisms and morbid obesity in the population of Extremadura (Spain)].

Objective: To select individuals whose morbid obesity can be attributed mainly to their individual genetic profile. After excluding patients with potential monogenic syndromes or diseases associated with obesity, we evaluated the association of the single nucleotide polymorphisms (SNPs) rs1861868 and rs9939609 of the fat-mass and obesity-associated FTO gene with an inherited predisposition to morbid obesity.

Patients And Methods: We evaluated 270 patients with morbid obesity and onset before the age of 14 years and selected 194 due to their phenotypes and family history; 289 control individuals were included.