TaSRO1 interacts with and suppresses TaSIP1 to fine tune mitochondrial retrograde signaling and enhance salinity stress tolerance
Ontology highlight
ABSTRACT:
ORGANISM(S): Triticum aestivum
PROVIDER: GSE156679 | GEO | 2022/09/01
REPOSITORIES: GEO
Similar Datasets
Project description:Nogo-A is a major player in neural development and regeneration, and it is the target of several clinical trials. However, its functions outside the nervous system are mostly unknown. We observed that Nogo-A is expressed in dental epithelial cells, responsible for the formation of enamel, and we showed that the deletion of Nogo-A in transgenic mouse models leads to the formation of defective enamel. We observed that Nogo-A directly interacts with molecules important for gene expression regulation, and its deletion perturbs their cellular localization. As a result, Nogo-A deletion induces overexpression of genes involved in cell differentiation and enamel production. Mechanistically, we demonstrated that intracellular Nogo-A, and not cell surface Nogo-A, is responsible for gene expression modulation. Taken together, our results indicate a new role for Nogo-A as regulator of enamel formation and suggest a new possible cell-autonomous function in regulating gene expression and cell differentiation.
2024-06-20 | PXD030386 | Pride
Project description:Phytochrome B (phyB) absorbs red light signals and subsequently initiates a set of molecular events in plant cells to promote photomorphogenesis. Here we show that phyB directly interacts with B-BOX CONTAINING PROTEIN 4 (BBX4), a positive regulator of red light signaling, and positively controls its abundance in red light. BBX4 associates with PHYTOCHROME INTERACTING FACTOR 3 (PIF3) and represses PIF3 transcriptional activation activity and PIF3-controlled gene expression. The degradation of BBX4 in darkness is dependent on CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) and the 26S proteasome system. Collectively, BBX4 acts as a key component of the phyB-PIF3-mediated signaling module and fine tunes the red light action. phyB promotes the accumulation of BBX4, which in turn serves to repress PIF3 action through direct physical interaction to promote photomorphogenic development in red light.
| S-EPMC6925995 | biostudies-literature
Project description:Mechanosensitive ion channels rely on membrane composition to transduce physical stimuli into electrical signals. The Piezo1 channel mediates mechanoelectrical transduction and regulates crucial physiological processes, including vascular architecture and remodeling, cell migration, and erythrocyte volume. The identity of the membrane components that modulate Piezo1 function remain largely unknown. Using lipid profiling analyses, we here identify dietary fatty acids that tune Piezo1 mechanical response. We find that margaric acid, a saturated fatty acid present in dairy products and fish, inhibits Piezo1 activation and polyunsaturated fatty acids (PUFAs), present in fish oils, modulate channel inactivation. Force measurements reveal that margaric acid increases membrane bending stiffness, whereas PUFAs decrease it. We use fatty acid supplementation to abrogate the phenotype of gain-of-function Piezo1 mutations causing human dehydrated hereditary stomatocytosis. Beyond Piezo1, our findings demonstrate that cell-intrinsic lipid profile and changes in the fatty acid metabolism can dictate the cell's response to mechanical cues.
| S-EPMC6416271 | biostudies-literature
Project description:Nitrate is a major nitrogen resource for plant growth and development and acts as both a crucial nutrient and a signaling molecule for plants; hence, understanding nitrate signaling is important for crop production. Abscisic acid (ABA) has been demonstrated to be involved in nitrate signaling, but the underlying mechanism is largely unknown in apple. In this study, we found that exogenous ABA inhibited the transport of nitrate from roots to shoots in apple, and the transcription of the nitrate transporter MdNRT1.5/MdNPF7.3 was noticeably reduced at the transcriptional level by ABA, which inhibited the transport of nitrate from roots to shoots. Then, it was found that the ABA-responsive transcription factor MdABI5 bound directly to the ABRE recognition site of the MdNRT1.5 promoter and suppressed its expression. Overexpression of MdABI5 inhibited ABA-mediated transport of nitrate from roots to shoots. Overall, these results demonstrate that MdABI5 regulates the transport of nitrate from roots to shoots partially by mediating the expression of MdNRT1.5, illuminating the molecular mechanism by which ABA regulates nitrate transport in apple.
| S-EPMC8558332 | biostudies-literature
Project description:Mechanical force applied along a disulfide bond alters its rate of reduction. We here aimed at quantifying the direct effect of force onto the chemical reactivity of a sulfur-sulfur bond in contrast to indirect, e.g., steric or mechanistic, influences. To this end, we evaluated the dependency of a disulfide bond's redox potential on a pulling force applied along the system. Our QM/MM simulations of cystine as a model system take conformational dynamics and explicit solvation into account and show that redox potentials increase over the whole range of forces probed here (30-3320 pN), and thus even in the absence of a significant disulfide bond elongation (<500 pN). Instead, at low forces, dihedrals and angles, as the softer degrees of freedom are stretched, contribute to the destabilization of the oxidized state. We find physiological forces to be likely to tune the disulfide's redox potentials to an extent similar to the tuning within proteins by point mutations.
| S-EPMC3274805 | biostudies-other
Project description:In budding yeast, the highly conserved small GTPase Cdc42 localizes to the cortex at a cell pole and orchestrates the trafficking and deposition of cell surface materials required for building a bud or mating projection (shmoo). Using a combination of quantitative imaging and mathematical modeling, we elucidate mechanisms of dynamic recycling of Cdc42 that balance diffusion. Rdi1, a guanine nucleotide dissociation inhibitor (GDI), mediates a fast recycling pathway, while actin patch-mediated endocytosis accounts for a slower one. These recycling mechanisms are restricted to the same region of the nascent bud, as both are coupled to the Cdc42 GTPase cycle. We find that a single dynamic parameter, the rate of internalization inside the window of polarized delivery, is tuned to give rise to distinct shapes of Cdc42 distributions that correlate with distinct morphogenetic fates, such as the formation of a round bud or a pointed shmoo.
| S-EPMC2805562 | biostudies-literature
Project description:Transcription of the human mitochondrial genome and correct processing of the two long polycistronic transcripts are crucial for oxidative phosphorylation. According to the tRNA punctuation model, nucleolytic processing of these large precursor transcripts occurs mainly through the excision of the tRNAs that flank most rRNAs and mRNAs. However, some mRNAs are not punctuated by tRNAs, and it remains largely unknown how these non-canonical junctions are resolved. The FASTK family proteins are emerging as key players in non-canonical RNA processing. Here, we have generated human cell lines carrying single or combined knockouts of several FASTK family members to investigate their roles in non-canonical RNA processing. The most striking phenotypes were obtained with loss of FASTKD4 and FASTKD5 and with their combined double knockout. Comprehensive mitochondrial transcriptome analyses of these cell lines revealed a defect in processing at several canonical and non-canonical RNA junctions, accompanied by an increase in specific antisense transcripts. Loss of FASTKD5 led to the most severe phenotype with marked defects in mitochondrial translation of key components of the electron transport chain complexes and in oxidative phosphorylation. We reveal that the FASTK protein family members are crucial regulators of non-canonical junction and non-coding mitochondrial RNA processing. Author summary As a legacy of their bacterial origin, mitochondria have retained their own genome with a unique gene expression system. All mitochondrially encoded proteins are essential components of the respiratory chain. Therefore, the mitochondrial gene expression is crucial for their iconic role as the ‘powerhouse of the cell’–ATP synthesis through oxidative phosphorylation. Consistently, defects in enzymes involved in this gene expression system are a common source of incurable inherited metabolic disorders, called mitochondrial diseases. The human mitochondrial transcription generates long polycistronic transcripts that carry information for multiple genes, so that the expression level of each gene is mainly regulated through post-transcriptional events. The polycistronic transcript first undergoes RNA processing, where individual mRNA, rRNA, and tRNA are cleaved off. However, its entire molecular mechanism remains unclear, and in particular, ‘non-canonical’ RNA processing has been poorly understood. To address this question, we studied the FASTK family proteins, emerging key mitochondrial post-transcriptional regulators. We generated different human cell lines carrying single or combined disruption of FASTKD3, FASTKD4, and FASTKD5 genes, and analyzed them using biochemical and genetic approaches. We show that the FASTK family members fine-tune the processing of both ‘canonical’ and ‘non-canonical’ mitochondrial RNA junctions.
| S-EPMC8601606 | biostudies-literature
Project description:Young children learn language at an incredible rate. Although children come prepared with powerful statistical-learning mechanisms, the statistics they encounter are also prepared for them: Children learn from caregivers motivated to communicate with them. How precisely do parents tune their speech to their children's individual language knowledge? To answer this question, we asked parent-child pairs (N = 41) to play a reference game in which the parents' goal was to guide their child to select a target animal from a set of three. Parents fine-tuned their referring expressions to their children's knowledge at the lexical level, producing more informative references for animals they thought their children did not know. Further, parents learned about their children's knowledge over the course of the game and tuned their referring expressions accordingly. Child-directed speech may thus support children's learning not because it is uniformly simplified but because it is tuned to individual children's language development.
| S-EPMC8641142 | biostudies-literature
Project description:CG-NAP, also known as AKAP450, is an anchoring/adaptor protein that streamlines signal transduction in various cell types by localizing signaling proteins and enzymes with their substrates. Great efforts are being devoted to elucidating functional roles of this protein and associated macromolecular signaling complex. Increasing understanding of pathways involved in regulating T lymphocytes suggests that CG-NAP can facilitate dynamic interactions between kinases and their substrates and thus fine-tune T cell motility and effector functions. As a result, new binding partners of CG-NAP are continually being uncovered. Here, we review recent advances in CG-NAP research, focusing on its interactions with kinases in T cells with an emphasis on the possible role of this anchoring protein as a target for therapeutic intervention in immune-mediated diseases.
| S-EPMC6861388 | biostudies-literature
Project description:Genome editing technologies not only provide unprecedented opportunities to study basic cellular system functionality but also improve the outcomes of several clinical applications. In this review, we analyze various gene editing techniques used to fine-tune immune systems from a basic research and clinical perspective. We discuss recent advances in the development of programmable nucleases, such as zinc-finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and clustered regularly interspaced short palindromic repeat (CRISPR)-Cas-associated nucleases. We also discuss the use of programmable nucleases and their derivative reagents such as base editing tools to engineer immune cells via gene disruption, insertion, and rewriting of T cells and other immune components, such natural killers (NKs) and hematopoietic stem and progenitor cells (HSPCs). In addition, with regard to chimeric antigen receptors (CARs), we describe how different gene editing tools enable healthy donor cells to be used in CAR T therapy instead of autologous cells without risking graft-versus-host disease or rejection, leading to reduced adoptive cell therapy costs and instant treatment availability for patients. We pay particular attention to the delivery of therapeutic transgenes, such as CARs, to endogenous loci which prevents collateral damage and increases therapeutic effectiveness. Finally, we review creative innovations, including immune system repurposing, that facilitate safe and efficient genome surgery within the framework of clinical cancer immunotherapies.
| S-EPMC7553077 | biostudies-literature