Negative feedback Dotaz Zobrazit nápovědu
- MeSH
- hypercholesterolemie MeSH
- kojenec MeSH
- metabolické nemoci MeSH
- nádory jater komplikace MeSH
- Check Tag
- kojenec MeSH
Plants adjust their growth according to gravity. Gravitropism involves gravity perception, signal transduction, and asymmetric growth response, with organ bending as a consequence [1]. Asymmetric growth results from the asymmetric distribution of the plant-specific signaling molecule auxin [2] that is generated by lateral transport, mediated in the hypocotyl predominantly by the auxin transporter PIN-FORMED3 (PIN3) [3-5]. Gravity stimulation polarizes PIN3 to the bottom sides of endodermal cells, correlating with increased auxin accumulation in adjacent tissues at the lower side of the stimulated organ, where auxin induces cell elongation and, hence, organ bending. A curvature response allows the hypocotyl to resume straight growth at a defined angle [6], implying that at some point auxin symmetry is restored to prevent overbending. Here, we present initial insights into cellular and molecular mechanisms that lead to the termination of the tropic response. We identified an auxin feedback on PIN3 polarization as underlying mechanism that restores symmetry of the PIN3-dependent auxin flow. Thus, two mechanistically distinct PIN3 polarization events redirect auxin fluxes at different time points of the gravity response: first, gravity-mediated redirection of PIN3-mediated auxin flow toward the lower hypocotyl side, where auxin gradually accumulates and promotes growth, and later PIN3 polarization to the opposite cell side, depleting this auxin maximum to end the bending. Accordingly, genetic or pharmacological interference with the late PIN3 polarization prevents termination of the response and leads to hypocotyl overbending. This observation reveals a role of auxin feedback on PIN polarity in the termination of the tropic response.
- MeSH
- Arabidopsis genetika růst a vývoj fyziologie MeSH
- gravitropismus * MeSH
- kyseliny indoloctové metabolismus MeSH
- percepce tíhy * MeSH
- proteiny huseníčku genetika metabolismus MeSH
- regulátory růstu rostlin metabolismus MeSH
- výhonky rostlin růst a vývoj MeSH
- zpětná vazba fyziologická MeSH
- Publikační typ
- časopisecké články MeSH
Signal transduction in biological cells is effected by signaling pathways that typically include multiple feedback loops. Here we analyze information transfer through a prototypical signaling module with biochemical feedback. The module switches stochastically between an inactive and active state; the input to the module governs the activation rate while the output (i.e., the product concentration) perturbs the inactivation rate. Using a novel perturbative approach, we compute the rate with which information about the input is gained from observation of the output. We obtain an explicit analytical result valid to first order in feedback strength and to second order in the strength of input. The total information gained during an extended time interval is found to depend on the feedback strength only through the total number of activation/inactivation events.
- MeSH
- biologické modely * MeSH
- gating iontového kanálu fyziologie MeSH
- lidé MeSH
- počítačová simulace MeSH
- signální transdukce fyziologie MeSH
- ukládání a vyhledávání informací metody MeSH
- vápník metabolismus MeSH
- vápníkové kanály metabolismus MeSH
- zpětná vazba fyziologická fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Plant-soil feedbacks (PSFs) and plant-plant competition influence performance and abundance of plants. To what extent the two biotic interactions are interrelated and thus affect plant performance in combination rather than in isolation remains poorly explored. It is also unclear how the abiotic context, such as resource availability, modifies individual and joint effects of PSFs and of plant-plant competition. Using a garden experiment, we assessed the strengths of PSFs, competition, and their combined effects explored under low and high nutrient levels, and related them to abundance of 46 plant species and their ecological optima with respect to soil nutrients. We found that PSFs reduced but did not eliminate differences in competitive ability of plant species. Isolated and combined effects of the biotic interactions poorly predicted local or regional abundance of species. They were rather related to species' ecological optima, as nutrient-demanding plants experienced less negative biotic effects but only in a nutrient-rich environment. Our study demonstrates that soil biota can mitigate differences in competitive ability among species. It remains to be tested whether such an equalizing effect can maintain coexistence under high nutrient availability, in which nutrient-demanding species may disproportionately benefit from less negative competition and PSF effects.
Wildlife monitoring using passive telemetry has become a robust method for investigating animal migration. With increased use, this method progressively pollutes the environment with technological waste represented by so called ghost tags (PIT tags ending in the environment due to reproductive expulsions, shedding or animal mortality). However, their presence in the environment may lead to failed detections of living individuals. We used tagging data from studies of the asp Leuciscus aspius and the bleak Alburnus alburnus collected from 2014 to 2018 and located ghost tag positions on the monitored spawning site using portable backpack reader for their detection. We modelled virtual river-wide flat-bed antennas (widths 0.2, 0.4, 0.6 and 0.8 m) representing monitoring effort and estimated the probability of the presence of ghost tags within the antenna field. Of 3724 PIT tags used in the study, we detected on the spawning ground 173 ghost tags originating from long-term monitoring. The ghost tags accumulated in the environment in time, suggesting insufficient degradation rate or shift downstream from the research site. Number of ghost tags present on the spawning ground led to high probability of disabled readings of tagged fish passing through the antenna electro-magnetic field. We demonstrate how accumulated ghost tags may cause detection failures for focal species and incomplete data acquisition. We infer that intensive long-term monitoring using PIT tag technology may encumber future data acquisition or entail additional costs for clean-up.
Auxin is unique among plant hormones due to its directional transport that is mediated by the polarly distributed PIN auxin transporters at the plasma membrane. The canalization hypothesis proposes that the auxin feedback on its polar flow is a crucial, plant-specific mechanism mediating multiple self-organizing developmental processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization. We performed microarray experiments to find regulators of this process that act downstream of auxin. We identified genes that were transcriptionally regulated by auxin in an AXR3/IAA17- and ARF7/ARF19-dependent manner. Besides the known components of the PIN polarity, such as PID and PIP5K kinases, a number of potential new regulators were detected, among which the WRKY23 transcription factor, which was characterized in more detail. Gain- and loss-of-function mutants confirmed a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly, processes requiring auxin-mediated PIN polarity rearrangements, such as vascular tissue development during leaf venation, showed a higher WRKY23 expression and required the WRKY23 activity. Our results provide initial insights into the auxin transcriptional network acting upstream of PIN polarization and, potentially, canalization-mediated plant development.
- MeSH
- Arabidopsis genetika růst a vývoj MeSH
- geneticky modifikované rostliny MeSH
- genové regulační sítě * účinky léků MeSH
- kořeny rostlin účinky léků genetika růst a vývoj metabolismus MeSH
- kyseliny indoloctové metabolismus farmakologie MeSH
- membránové transportní proteiny genetika metabolismus MeSH
- mikročipová analýza MeSH
- polarita buněk * genetika MeSH
- proteiny huseníčku genetika metabolismus fyziologie MeSH
- regulace genové exprese u rostlin účinky léků MeSH
- stanovení celkové genové exprese MeSH
- transkripční faktory fyziologie MeSH
- zpětná vazba fyziologická účinky léků MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
IL-17 mediates immune protection from fungi and bacteria, as well as it promotes autoimmune pathologies. However, the regulation of the signal transduction from the IL-17 receptor (IL-17R) remained elusive. We developed a novel mass spectrometry-based approach to identify components of the IL-17R complex followed by analysis of their roles using reverse genetics. Besides the identification of linear ubiquitin chain assembly complex (LUBAC) as an important signal transducing component of IL-17R, we established that IL-17 signaling is regulated by a robust negative feedback loop mediated by TBK1 and IKKε. These kinases terminate IL-17 signaling by phosphorylating the adaptor ACT1 leading to the release of the essential ubiquitin ligase TRAF6 from the complex. NEMO recruits both kinases to the IL-17R complex, documenting that NEMO has an unprecedented negative function in IL-17 signaling, distinct from its role in NF-κB activation. Our study provides a comprehensive view of the molecular events of the IL-17 signal transduction and its regulation.
- MeSH
- adaptorové proteiny signální transdukční genetika metabolismus MeSH
- HEK293 buňky MeSH
- HeLa buňky MeSH
- kinasa I-kappa B genetika metabolismus MeSH
- lidé MeSH
- protein-serin-threoninkinasy genetika metabolismus MeSH
- receptory interleukinu-17 genetika metabolismus MeSH
- signální transdukce * MeSH
- zpětná vazba fyziologická * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Cell-autonomous induction of type I interferon must be stringently regulated. Rapid induction is key to control virus infection, whereas proper limitation of signaling is essential to prevent immunopathology and autoimmune disease. Using unbiased kinome-wide RNAi screening followed by thorough validation, we identified 22 factors that regulate RIG-I/IRF3 signaling activity. We describe a negative-feedback mechanism targeting RIG-I activity, which is mediated by death associated protein kinase 1 (DAPK1). RIG-I signaling triggers DAPK1 kinase activation, and active DAPK1 potently inhibits RIG-I stimulated IRF3 activity and interferon-beta production. DAPK1 phosphorylates RIG-I in vitro at previously reported as well as other sites that limit 5'ppp-dsRNA sensing and virtually abrogate RIG-I activation.
- MeSH
- buňky A549 MeSH
- fosforylace MeSH
- HEK293 buňky MeSH
- kultivované buňky MeSH
- lidé MeSH
- malá interferující RNA genetika MeSH
- myši MeSH
- proteinkinasy asociované se smrtí metabolismus MeSH
- proteinkinasy metabolismus MeSH
- receptory kyseliny retinové metabolismus MeSH
- signální transdukce MeSH
- zpětná vazba fyziologická MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
