RNA editing is converting hundreds of cytosines into uridines during organelle gene expression of land plants. The pentatricopeptide repeat (PPR) proteins are at the core of this posttranscriptional RNA modification. Even if a PPR protein defines the editing site, a DYW domain of the same or another PPR protein is believed to catalyze the deamination. To give insight into the organelle RNA editosome, we performed tandem affinity purification of the plastidial CHLOROPLAST BIOGENESIS 19 (CLB19) PPR editing factor. Two PPR proteins, dually targeted to mitochondria and chloroplasts, were identified as potential partners of CLB19. These two proteins, a P-type PPR and a member of a small PPR-DYW subfamily, were shown to interact in yeast. Insertional mutations resulted in embryo lethality that could be rescued by embryo-specific complementation. A transcriptome analysis of these complemented plants showed major editing defects in both organelles with a very high PPR type specificity, indicating that the two proteins are core members of E+-type PPR editosomes.
The mitochondrial carrier uncoupling protein (UCP) 2 belongs to the family of the UCPs. Despite its name, it is now accepted that UCP2 is rather a metabolite transporter than a UCP. UCP2 can regulate oxidative stress and/or energetic metabolism. In rodents, UCP2 is involved in the control of α- and β-cell mass as well as insulin and glucagon secretion. Our aim was to determine whether the effects of UCP2 observed on β-cell mass have an embryonic origin. Thus, we used knockout mice. We found an increased size of the pancreas in fetuses at embryonic day 16.5, associated with a higher number of α- and β-cells. This phenotype was caused by an increase of PDX1 progenitor cells. Perinatally, an increase in the proliferation of endocrine cells also participates in their expansion. Next, we analyzed the oxidative stress in the pancreata. We quantified an increased nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) in the mutant, suggesting an increased production of reactive oxygen species (ROS). Phosphorylation of AKT, an ROS target, was also activated in the pancreata. Finally, administration of the antioxidant -acetyl-l-cysteine to pregnant mice alleviated the effect of knocking out UCP2 on pancreas development. Together, these data demonstrate that UCP2 controls pancreas development through the ROS-AKT signaling pathway.
Among the basal ganglia nuclei, the subthalamic nucleus (STN) is considered to play a major role in output modulation. The STN represents a relay of the motor cortico-basal ganglia-thalamo-cortical circuit and has become the standard surgical target for treating Parkinson's patients with long-term motor fluctuations and dyskinesia. But chronic bilateral stimulation of the STN produces cognitive effects. According to animal and clinical studies, the STN also appears to have direct or indirect connections with the frontal associative and limbic areas. This prospective study was conducted to analyse regional cerebral blood flow changes in single-photon emission computed tomography imaging of six Parkinson's patients before and after STN stimulation. We particularly focused on the dorsolateral prefrontal cortex and the frontal limbic areas using a manual anatomical MRI segmentation method. We defined nine regions of interest, segmenting each MR slice to quantify the regional cerebral blood flow on pre- and postoperative SPECT images. We normalised the region-of-interest-based measurements to the entire brain volume. The patients showed increased activation during STN stimulation in the dorsolateral prefrontal cortex bilaterally and no change in the anterior cingulate and orbito-frontal cortices. In our study, STN stimulation induced activation of premotor and associative frontal areas. Further studies are needed to underline involvement of the STN with the so-called limbic system.
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