The transition from vegetative growth to flower formation is critical for the survival of flowering plants. The plant-specific transcription factor LEAFY (LFY) has central, evolutionarily conserved roles in this process, both in the formation of the first flower and later in floral patterning. We performed genome-wide binding and expression studies to elucidate the molecular mechanisms by which LFY executes these roles. Our study reveals that LFY directs an intricate regulatory network in control of floral homeotic gene expression and, unexpectedly, controls the expression of genes regulating the response to external stimuli in Arabidopsis. We further show that LFY dampens responses to a bacterial MAMP (microbe-associated molecular pattern) and to pathogen challenge. Our findings suggest a molecular mechanism for the coordination of reproductive stage development and disease response programs in plants. Regulation of these distinct survival programs by a single transcription factor may ensure optimal allocation of plant resources for reproductive fitness.
LEAFY target genes reveal floral regulatory logic, cis motifs, and a link to biotic stimulus response.
Specimen partView Samples
Paf1 and Ski8 were selected as representative subunits of the Paf1 complex (PAF1C), and RNA-seq analysis was performed in triplicate to compare the genes affected by Paf1, Ski8, and Rtf1 knockdown in HeLa cells. Overall design: Total RNA was harvested from control HeLa and Ski8 knockdown cells at day 4 and from Rtf1 or Paf1 knockdown cells at day 7 and was subjected to RNA-seq in triplicates.
Correction for Cao et al., Characterization of the Human Transcription Elongation Factor Rtf1: Evidence for Nonoverlapping Functions of Rtf1 and the Paf1 Complex.
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The NGS-associated mRNA-seq analysis was conducted to survey transcriptome changes responding to three UPR inducers (tunicamycin, DTT, & Azetidine-2-cytosine) by four double mutant of three UPR-associated transcription factors (bZIP17, bZIP28, & bZIP60) and two activators (S1P & S2P). Overall design: Four double mutant lines (bz17/28, bz28/60, bz17/60, and s1p/s2p) were subjected to the analysis.
ER-Anchored Transcription Factors bZIP17 and bZIP28 Regulate Root Elongation.
Age, Specimen part, SubjectView Samples
To identify the transcripts fractionated into microsome fraction in ribosome-independent manner, we isolate rough microsome fraction by sucrose density gradient ultracengrifugation, then the rough microsome fraction is centrifugated following treatment with puromycine and EDTA in high-salt buffer to remove ribosomes. The pellet and surpernatant are named naked microsome fraction (NM) and stripped ribosome fraction (SR), respectively. By calculating the ratio of the level of each mRNA in NM and SR, we identify the enriched transcripts in NM. Overall design: Transcript profiles of subcellular fractions from S2-DRSC Drosophila cultured cell
Control of tissue size and development by a regulatory element in the <i>yorkie</i> 3'UTR.
Purpose: Characterize the role of the coactivator subunit TAF9b during differentiation of embryonic stem cells into motor neurons as well in mouse newborn spinal column tissues. Overall design: RNA-seq comparing WT and TAF9B KO mouse ES cells differentiated into motor neurons. RNA-seq comparing WT and TAF9B KO mouse newborn spinal column tissues. ChIP-seq mapping TAF9b and RNA Pol II binding sites in in vitro differentiated motor neurons.
Core promoter factor TAF9B regulates neuronal gene expression.
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The purpose of this study was to isolate NCSCs from oral mucosa using the neurosphere technique.
Sphere-Derived Multipotent Progenitor Cells Obtained From Human Oral Mucosa Are Enriched in Neural Crest Cells.
Sex, Age, Specimen partView Samples
To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a danger signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a calm down signal.
Immunosuppression via adenosine receptor activation by adenosine monophosphate released from apoptotic cells.
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For victims of radiological accidents, rapid dose estimation and damage prediction are essential. Administering the gold-standard biodosimetry chromosome aberration assay requires highly skilled individuals and several days of labor; consequently, rapid turnaround is an important concern. Identification of new dose estimation markers and damage-predicting in vivo molecules to replace the chromosome aberration assay is crucial to improving the delivery time of medical treatment. Here, we investigated the applicability of mRNA levels using a mouse model. Female C57BL/6J mice were X-ray irradiated at various doses, and a DNA microarray was then performed to identify differentially expressed mRNAs in whole blood. The microarray analysis identified 14 radioresponsive mRNAs with more than fourfold differences by pattern matching in the expression at 24 h postirradiation. In particular, mRNA expression of Slfn4, Itgb5, Smim3, Tmem40, Litaf, Gp1bb and Cxx1c was significantly increased in a radiation-dose-dependent manner, as validated by reverse transcription quantitative polymerase chain reaction. We also performed an analysis using the cBioPortal for Cancer Genomics and found that the overall survival of ovarian adenocarcinoma patients with alterations in Smim3 and that of thymoma patients with alterations in Cxx1c had a worse prognosis than patients without these alterations. These findings suggest that the expression of several genes in whole blood was a sensitive and specific biomarker of radiation exposure and can be used as a rapid and reliable prospective molecular biomarker in radiological emergencies.
Identification of Radiation-Dose-Dependent Expressive Genes in Individuals Exposed to External Ionizing Radiation.
Sex, Age, Specimen part, TreatmentView Samples
Genomic imprinting is an allele-specific gene expression system important for mammalian development and function. The molecular basis of genomic imprinting is allele-specific DNA methylation 2. While it is well known that the de novo DNA methyltransferases Dnmt3a/b are responsible for the establishment of genomic imprinting, how the methylation mark is erased during primordial germ cell (PGC) reprogramming remains a mystery. Here we report that Tet1 plays a critical role in the erasure of genomic imprinting. We show that despite their identical genotype, progenies derived from mating between Tet1-KO males and wild-type females exhibit a number of variable phenotypes including placental, fetal and postnatal growth defects, and early embryonic lethality. These defects are, at least in part, caused by the dysregulation of imprinted genes, such as Peg10 and Peg3, which exhibit aberrant hypermethylation in the paternal allele of differential methylated regions (DMRs). RNA-seq reveals extensive dysregulation of imprinted genes in the next generation due to paternal functional loss of Tet1. Genome-wide DNA methylation analysis of E13.5 PGCs and sperm derived from Tet1-KO mice reveals hypermethylation of DMRs of imprinted genes in sperm, which can be traced back to PGCs. Dynamics of methylation change in Tet1-affected sites suggested that Tet1 swipes remaining methylation including imprinted genes at late reprogramming stage. We also revealed that Tet1play a role in paternal imprinting erasure in females germline. Thus, our study establishes a critical function for Tet1 in the erasure of genomic imprinting. Overall design: Gene expression analysis of E9.5 embryos
Role of Tet1 in erasure of genomic imprinting.
Specimen part, SubjectView Samples