Ion antiport accelerates photosynthetic acclimation in fluctuating light environments

Many photosynthetic organisms globally, including crops, forests and algae, must grow in environments where the availability of light energy fluctuates dramatically. How photosynthesis maintains high efficiency despite such fluctuations in its energy source remains poorly understood. Here we show that Arabidopsis thaliana ​K+ efflux antiporter (​KEA3) is critical for high photosynthetic efficiency under fluctuating light. On a shift from dark to low light, or high to low light, ​kea3 mutants show prolonged dissipation of absorbed light energy as heat. ​KEA3 localizes to the thylakoid membrane, and allows proton efflux from the thylakoid lumen by proton/potassium antiport. ​KEA3’s activity accelerates the downregulation of pH-dependent energy dissipation after transitions to low light, leading to faster recovery of high photosystem II quantum efficiency and increased ​CO2 assimilation. Our results reveal a mechanism that increases the efficiency of photosynthesis under fluctuating light. [EN]This project was funded by the Carnegie Institution for Science, by ERDF-cofinanced grants from the Ministry of Economy and Competitiveness (BIO2012-33655) and Junta de Andalucia (CVI-7558) to K.V., the Natural Sciences and Engineering Research Council of Canada (NSERC) PGS-D3 scholarship to L.P. and Deutsche Forschungsgemeinschaft grants (JA 665/10-1 and GRK 1525 to P.J.; AR 808/1-1 to U.A.).Peer reviewe

A study protocol for a pilot randomized controlled trial to evaluate the effectiveness of a gene-based nutrition and lifestyle recommendation for weight management among adults: the MyGeneMyDiet® study

IntroductionManaging nutrition and lifestyle practices, nutrition phenotypes, and the genome forms the foundation of precision nutrition. Precision nutrition focuses on metabolic variability among individuals, and one approach to achieving its goals is to integrate gene-based nutrition and lifestyle recommendations in nutrition practice. However, scientific evidence proving the effectiveness of such recommendations is limited. This study will examine whether providing nutrition and lifestyle recommendations based on individual genotype can lead to better weight loss, along with reduction in body mass index (BMI), waist circumference, and body fat percentage among overweight and obese adults.Methods and analysisA parallel group, single-blind, randomized controlled trial will be conducted. Sixty-two overweight/obese individuals aged 19–59 years old will be recruited. Participants will be randomly allocated to either the intervention (n = 31) or the control arm (n = 31). Participants in the intervention group will receive the MyGeneMyDiet® Recommendation for Weight Management, a gene-based nutrition and lifestyle recommendation that was developed based on existing evidence of the effects of FTO rs9939609 on body weight, BMI, and physical activity; UCP1 rs1800592 on calorie intake; and TCF7L2 rs7903146 on dietary fat intake. Participants in the control group will receive the standard recommendations for weight management. The primary outcomes will be the differences in weight, BMI, waist circumference, and body fat percentage between arms in both the active phase (6 months) and inactive phase (last 6 months) of the trial. Participants in both arms will be evaluated at baseline and in months 3, 6, 9, and 12.DiscussionTo the best of our knowledge, this will be the first gene-based intervention that will adopt a phase of intensive nutrition counseling, followed by a simulation of a free-living state to determine adherence to a gene-based recommendation. This study will contribute to the future implementation of precision nutrition interventions by providing evidence on the effectiveness of a gene-based nutrition and lifestyle recommendation for weight loss.Clinical trial registrationclinicaltrials.gov, identifier [NCT05098899]

Circadian dysfunction in the Q175 model of Huntington's disease: Network analysis.

Disturbances in sleep/wake cycle are a common complaint of individuals with Huntington's disease (HD) and are displayed by HD mouse models. The underlying mechanisms, including the possible role of the circadian timing system, have been the topic of a number of recent studies. The (z)Q175 mouse is a knock-in model in which the human exon 1 sequence of the huntingtin gene is inserted into the mouse DNA with approximately 190 CAG repeats. Among the numerous models available, the heterozygous Q175 offers strong construct validity with a single copy of the mutation, genetic precision of the insertion and control of mutation copy number. In this review, we will summarize the evidence that this model exhibits disrupted diurnal and circadian rhythms in locomotor activity. We found overwhelming evidence for autonomic dysfunction including blunted daily rhythms in heart rate and core body temperature (CBT), reduced heart rate variability, and almost a complete failure of the sympathetic arm of the autonomic nervous system to function during the baroreceptor reflex. Mechanistically, the Q175 mouse model exhibits deficits in the neural output of the central circadian clock, the suprachiasmatic nucleus along with an enhancement of at least one type of potassium current in these neurons. Finally, we report a novel network analysis examining the phase coherence between activity, CBT, and cardiovascular measures. Such analyses found that even young Q175 mutants (heterozygous or homozygous) show coherence degradation, and suggests that loss of phase coherence is a variable that should be considered as a possible biomarker for HD