ABERRANT PANICLE ORGANIZATION 1 temporally regulates meristem identity in rice

AbstractWe report a recessive mutation of rice, aberrant panicle organization 1 (apo1), which severely affects inflorescence architecture, floral organ identity, and leaf production rate. In the wild-type inflorescence, the main-axis meristem aborts after forming 10–12 primary branch primordia. However, in apo1, the main-axis meristem was converted to a spikelet meristem after producing a small number of branch primordia. In addition, the branch meristems in apo1 became spikelet meristems earlier than in wild type. Therefore, in the inflorescence, the apo1 mutation caused the precocious conversion of the meristem identity. In the apo1 flower, lodicules were increased at the expense of stamens, and carpels were formed indeterminately by the loss of meristem determinacy. Vegetative development is also affected in the apo1. Leaves were formed rapidly throughout the vegetative phase, indicating that APO1 is also involved in temporal regulation of leaf production. These phenotypes suggest that the APO1 plays an important role in the temporal regulation of both vegetative and reproductive development

Wireless optogenetics protects against obesity via stimulation of non-canonical fat thermogenesis.

Cold stimuli and the subsequent activation of β-adrenergic receptor (β-AR) potently stimulate adipose tissue thermogenesis and increase whole-body energy expenditure. However, systemic activation of the β3-AR pathway inevitably increases blood pressure, a significant risk factor for cardiovascular disease, and, thus, limits its application for the treatment of obesity. To activate fat thermogenesis under tight spatiotemporal control without external stimuli, here, we report an implantable wireless optogenetic device that bypasses the β-AR pathway and triggers Ca2+ cycling selectively in adipocytes. The wireless optogenetics stimulation in the subcutaneous adipose tissue potently activates Ca2+ cycling fat thermogenesis and increases whole-body energy expenditure without cold stimuli. Significantly, the light-induced fat thermogenesis was sufficient to protect mice from diet-induced body-weight gain. The present study provides the first proof-of-concept that fat-specific cold mimetics via activating non-canonical thermogenesis protect against obesity

Development of a low-alpha-emitting {\mu}-PIC for NEWAGE direction-sensitive dark-matter search

NEWAGE is a direction-sensitive dark-matter-search experiment that uses a micro-patterned gaseous detector, or {\mu}-PIC, as the readout. The main background sources are {\alpha}-rays from radioactive contaminants in the {\mu}-PIC. We have therefore developed a low-alpha-emitting {\mu}-PICs and measured its performances. We measured the surface {\alpha}-ray emission rate of the {\mu}-PIC in the Kamioka mine using a surface {\alpha}-ray counter based on a micro TPC.Comment: 6 pages, 4 figure

Mitochondrial lipoylation integrates age-associated decline in brown fat thermogenesis.

Thermogenesis in brown adipose tissue (BAT) declines with age; however, what regulates this process remains poorly understood. Here, we identify mitochondria lipoylation as a previously unappreciated molecular hallmark of aged BAT in mice. Using mitochondrial proteomics, we show that mitochondrial lipoylation is disproportionally reduced in aged BAT through a post-transcriptional decrease in the iron-sulfur (Fe-S) cluster formation pathway. A defect in the Fe-S cluster formation by the fat-specific deletion of Bola3 significantly reduces mitochondrial lipoylation and fuel oxidation in BAT, leading to glucose intolerance and obesity. In turn, enhanced mitochondrial lipoylation by α-lipoic acid supplementation effectively restores BAT function in old mice, thereby preventing age-associated obesity and glucose intolerance. The effect of α-lipoic acids requires mitochondrial lipoylation via the Bola3 pathway and does not depend on the anti-oxidant activity of α-lipoic acid. These results open up the possibility to alleviate the age-associated decline in energy expenditure by enhancing the mitochondrial lipoylation pathway

Neurobiology of Depression and Anxiety in Parkinson's Disease

Depression and anxiety are common in Parkinson's disease (PD) and have important consequences on quality of life. These have long been recognized as frequent accompanying syndromes of PD, and several reports suggest that these are the causative process or risk factors that are present many years before the appearance of motor symptoms. The neurochemical changes in PD involving dopamine, norepinephrine, and serotonin might be related to the pathophysiology of depression and anxiety, but this is still not clear. Several studies showed that anxiety in PD patients occurs earlier than depression, during premotor phase, suggesting that there may be a link between the mechanisms that cause anxiety and PD. Whereas a recent study reported that PD patients with depression and anxiety were associated with different demographic and clinical features