TL;DR: It is found that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene and suggests that the deregulation of this process may underlie the pathology of RT T.
Abstract: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T
TL;DR: In bioluminescent bacteria growing in shake flasks, the enzyme luciferase has been shown to be synthesized in a relatively short burst during the period of exponential growth, attributed to a stimulation of existing patterns of synthesis.
Abstract: In bioluminescent bacteria growing in shake flasks, the enzyme luciferase has been shown to be synthesized in a relatively short burst during the period of exponential growth. The luciferase gene appears to be completely inactive in a freshly inoculated culture; the pulse of preferential luciferase synthesis which occurs later is the consequence of its activation at the level of deoxyribonucleic acid transcription which is attributed to an effect of a “conditioning” of the medium by the growing of cells. Although cells grown in a minimal medium also exhibit a similar burst of synthesis of the luminescent system, the amount of synthesis is quantitatively less, relative to cell mass. Under such conditions, added arginine results in a striking stimulation of bioluminescence. This is attributed to a stimulation of existing patterns of synthesis and not to induction or derepression per se.
TL;DR: Brassinosteroids compensate for different cell elongation defects of Arabidopsis det, cop, fus, and axr2 mutants, indicating that these steroids play an essential role in the regulation of plant development.
TL;DR: An Arabidopsis thaliana line that is mutant for the R2R3 MYB gene, AtMYB4, shows enhanced levels of sinapate esters in its leaves, indicating that derepression is an important mechanism for acclimation to UV‐B in A.thaliana.
Abstract: An Arabidopsis thaliana line that is mutant for the R2R3 MYB gene, AtMYB4, shows enhanced levels of sinapate esters in its leaves. The mutant line is more tolerant of UV-B irradiation than wild type. The increase in sinapate ester accumulation in the mutant is associated with an enhanced expression of the gene encoding cinnamate 4-hydroxylase, which appears to be the principal target of AtMYB4 and an effective rate limiting step in the synthesis of sinapate ester sunscreens. AtMYB4 expression is downregulated by exposure to UV-B light, indicating that derepression is an important mechanism for acclimation to UV-B in A.thaliana. The response of target genes to AtMYB4 repression is dose dependent, a feature that operates under physiological conditions to reinforce the silencing effect of AtMYB4 at high activity. AtMYB4 works as a repressor of target gene expression and includes a repression domain. It belongs to a novel group of plant R2R3 MYB proteins involved in transcriptional silencing. The balance between MYB activators and repressors on common target promoters may provide extra flexibility in transcriptional control.
TL;DR: EIN3/EIL1 is identified as a key integration node whose activation requires both JA and ET signaling, and transcriptional derepression is illustrated as a common mechanism to integrate diverse signaling pathways in the regulation of plant development and defense.
Abstract: Jasmonate (JA) and ethylene (ET) are two major plant hormones that synergistically regulate plant development and tolerance to necrotrophic fungi Both JA and ET induce the expression of several pathogenesis-related genes, while blocking either signaling pathway abolishes the induction of these genes by JA and ET alone or in combination However, the molecular basis of JA/ET coaction and signaling interdependency is largely unknown Here, we report that two Arabidopsis ET-stabilized transcription factors (EIN3 and EIL1) integrate ET and JA signaling in the regulation of gene expression, root development, and necrotrophic pathogen defense Further studies reveal that JA enhances the transcriptional activity of EIN3/EIL1 by removal of JA-Zim domain (JAZ) proteins, which physically interact with and repress EIN3/EIL1 In addition, we find that JAZ proteins recruit an RPD3-type histone deacetylase (HDA6) as a corepressor that modulates histone acetylation, represses EIN3/EIL1-dependent transcription, and inhibits JA signaling Our studies identify EIN3/EIL1 as a key integration node whose activation requires both JA and ET signaling, and illustrate transcriptional derepression as a common mechanism to integrate diverse signaling pathways in the regulation of plant development and defense