29 research outputs found
Studies on the antagonistic effect of rhizobacteria against soilborne Phytophthora species on strawberry
No full text[no abstract
Studies on efficacy and mode of action of rhizosphere bacteria against Phytophthora spp. in strawberry
No full textAfter screening of several rhizosphere bacteria against the soilborne pathogens of red core and crown rot disease of strawberry Phytophthora fragariae var. fragariae and Phytophthora cactorum under in vitro conditions, three of the most active isolates such as Raoultella terrigena (G- 584), Bacillus amyloliquefaciens (G-V1) and Pseudomonas fluorescens (2R1-7) were selected for further studies under in vivo conditions. In greenhouse and field experiments, the three isolates were tested against both Phytophthora diseases under artificial infested soil conditions. Root dip treatment with these bacterial antagonists produced a control effect on both fungal diseases up to 55% and were nearly comparable with the chemical fungicide Aliette. First studies on the mode of action of antagonists showed differences in enzymatic reaction
Biological control of red core (Phytophthora fragariae var. fragariae) and crown rot (P. cactorum) disease of strawberry by bacterial antagonists
No full textRegulation of entry into gametogenesis by Ste11: the endless game.
No full textSexual reproduction is a fundamental aspect of eukaryotic cells, and a conserved feature of gametogenesis is its dependency on a master regulator. The ste11 gene was isolated more than 20 years ago by the Yamamoto laboratory as a suppressor of the uncontrolled meiosis driven by a pat1 mutant. Numerous studies from this laboratory and others have established the role of the Ste11 transcription factor as the master regulator of the switch between proliferation and differentiation in fission yeast. The transcriptional and post-transcriptional controls of ste11 expression are intricate, but most are not redundant. Whereas the transcriptional controls ensure that the gene is transcribed at a high level only when nutrients are rare, the post-transcriptional controls restrict the ability of Ste11 to function as a transcription factor to the G1-phase of the cell cycle from where the differentiation programme is initiated. Several feedback loops ensure that the cell fate decision is irreversible. The complete panel of molecular mechanisms operating to warrant the timely expression of the ste11 gene and its encoded protein basically mirrors the advances in the understanding of the numerous ways by which gene expression can be modulated.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe
Regulation of entry into gametogenesis by Ste11: the endless game
No full textAbstract Sexual reproduction is a fundamental aspect of eukaryotic cells, and a conserved feature of gametogenesis is its dependency on a master regulator. The ste11 gene was isolated more than 20 years ago by the Yamamoto laboratory as a suppressor of the uncontrolled meiosis driven by a pat1 mutant. Numerous studies from this laboratory and others have established the role of the Ste11 transcription factor as the master regulator of the switch between proliferation and differentiation in fission yeast. The transcriptional and post-transcriptional controls of ste11 expression are intricate, but most are not redundant. Whereas the transcriptional controls ensure that the gene is transcribed at a high level only when nutrients are rare, the post-transcriptional controls restrict the ability of Ste11 to function as a transcription factor to the G 1 -phase of the cell cycle from where the differentiation programme is initiated. Several feedback loops ensure that the cell fate decision is irreversible. The complete panel of molecular mechanisms operating to warrant the timely expression of the ste11 gene and its encoded protein basically mirrors the advances in the understanding of the numerous ways by which gene expression can be modulated
Uncoupling transcription from covalent histone modification.
No full textIt is widely accepted that transcriptional regulation of eukaryotic genes is intimately coupled to covalent modifications of the underlying chromatin template, and in certain cases the functional consequences of these modifications have been characterized. Here we present evidence that gene activation in the silent heterochromatin of the yeast Saccharomyces cerevisiae can occur in the context of little, if any, covalent histone modification. Using a SIR-regulated heat shock-inducible transgene, hsp82-2001, and a natural drug-inducible subtelomeric gene, YFR057w, as models we demonstrate that substantial transcriptional induction (>200-fold) can occur in the context of restricted histone loss and negligible levels of H3K4 trimethylation, H3K36 trimethylation and H3K79 dimethylation, modifications commonly linked to transcription initiation and elongation. Heterochromatic gene activation can also occur with minimal H3 and H4 lysine acetylation and without replacement of H2A with the transcription-linked variant H2A.Z. Importantly, absence of histone modification does not stem from reduced transcriptional output, since hsp82-ΔTATA, a euchromatic promoter mutant lacking a TATA box and with threefold lower induced transcription than heterochromatic hsp82-2001, is strongly hyperacetylated in response to heat shock. Consistent with negligible H3K79 dimethylation, dot1Δ cells lacking H3K79 methylase activity show unimpeded occupancy of RNA polymerase II within activated heterochromatic promoter and coding regions. Our results indicate that large increases in transcription can be observed in the virtual absence of histone modifications often thought necessary for gene activation
Histone H2B ubiquitylation represses gametogenesis by opposing RSC-dependent chromatin remodeling at the ste11 master regulator locus
No full textIn fission yeast, the ste11 gene encodes the master regulator initiating the switch from vegetative growth to gametogenesis. In a previous paper, we showed that the methylation of H3K4 and consequent promoter nucleosome deacetylation repress ste11 induction and cell differentiation (Materne et al., 2015) but the regulatory steps remain poorly understood. Here we report a genetic screen that highlighted H2B deubiquitylation and the RSC remodeling complex as activators of ste11 expression. Mechanistic analyses revealed more complex, opposite roles of H2Bubi at the promoter where it represses expression, and over the transcribed region where it sustains it. By promoting H3K4 methylation at the promoter, H2Bubi initiates the deacetylation process, which decreases chromatin remodeling by RSC. Upon induction, this process is reversed and efficient NDR (nucleosome depleted region) formation leads to high expression. Therefore, H2Bubi represses gametogenesis by opposing the recruitment of RSC at the promoter of the master regulator ste11 gene.This work was supported by grant BFU2014-52143-P from the Spanish Ministerio
de Economía y Competitividad to FA and by grants PR T.0012.14, MIS F.4523.11, Ceruna and Marie Curie Action to DH. DH is a FNRS Senior Research Associate.Peer Reviewe
Heterochromatic gene activation occurs in the context of minimal transcription-linked H3 methylation and is unimpaired by ablation of Dot1.
No full text<p>(a) H3K56ac ChIP analysis of <i>hsp82-2001</i> in <i>sir4Δ</i> or <i>SIR<sup>+</sup></i> cells subjected to an instantaneous 30° to 39°C thermal upshift for the times indicated. Quantification was done using Real Time qPCR. The acetylated H3K56/Myc-H4 quotient of the non-induced <i>sir4Δ</i> sample was set to 1.0 for each amplicon. PTM-specific and Myc-H4 signals at the heat shock transgene were normalized to those measured at <i>PMA1</i> and <i>ARS504</i>, respectively. Shown are means ± S.D. (N = 2; qPCR = 4). (b) H3K36me3 ChIP analysis of <i>hsp82-2001</i> conducted as in A. (c) H3K4me3 ChIP analysis of <i>hsp82-2001</i> in <i>sir4Δ</i> or <i>SIR<sup>+</sup></i> cells subjected to an instantaneous 30° to 39°C thermal upshift for the times indicated. Quantification and scaling were done as in A, except H3K4me3/H3 quotients are depicted, and both PTM-specific and H3 signals were normalized to those measured at <i>ARS504</i>. Shown are means ± S.D. (N = 2; qPCR = 4). (d) H3K79me2 ChIP analysis of <i>hsp82-2001</i> in <i>sir4Δ</i> or <i>SIR<sup>+</sup></i> cells as in C. (e) Pol II ChIP analysis of heterochromatic <i>hsp82-2001</i> in <i>DOT1<sup>+</sup></i> and <i>dot1Δ</i> strains subjected to heat shock as above. Pol II occupancy was determined using ChIP-qPCR as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1004202#pgen-1004202-g003" target="_blank">Figure 3A</a>. Shown are means ± S.D. (N = 2; qPCR = 4).</p
Transcriptional activation of the subtelomeric <i>YFR057w</i> gene is unlinked to covalent histone modification.
No full text<p>(a) <i>YFR057w</i> mRNA levels in <i>SIR<sup>+</sup></i> and <i>sir2Δ</i> cells (BY4741 background) exposed to 200 µg/ml cycloheximide (CX) for the indicated times. <i>YFR057w</i> transcripts were quantified by RT-qPCR, and normalized to those of <i>SCR1</i>. Depicted are means ± S.D. (N = 3; qPCR = 6). (b) ChIP-qPCR analysis of Pol II within the <i>YFR057w</i> promoter and ORF in <i>sir2Δ</i> and <i>SIR<sup>+</sup></i> cells exposed to cycloheximide for the indicated times as in A. Pol II occupancy was determined as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1004202#pgen-1004202-g003" target="_blank">Figure 3A</a>. Occupancy of the non-induced promoter (<i>sir2Δ</i>) was set to 1.0; all other occupancies (both promoter and ORF) are scaled relative to it. Depicted are means ± S.D. (N = 4; qPCR = 8). (c) ChIP-qPCR analysis of histone PTMs within the <i>YFR057w</i> promoter (H3K18ac, H4K16ac, H3K4me2,3) or ORF (H3K79me2) in <i>sir2Δ</i> and <i>SIR<sup>+</sup></i> cells exposed for the indicated times to cycloheximide as in A. Shown are normalized PTM/histone H3 quotients. PTM-specific and H3 signals at <i>YFR057w</i> were normalized to those measured at <i>PMA1</i> and <i>ARS504</i>, respectively. The PTM/histone H3 quotient of the non-induced <i>sir2Δ</i> sample was set to 1.0 in each case. Depicted are means ± S.D. (N = 2; qPCR = 4). (d) ChIP-qPCR analysis of H3K36me3 enrichment within the ORF and Htz1 enrichment within the promoter as in C, for the indicated times following addition of cycloheximide (N = 2; qPCR = 4). (e) As in D, except H3K56ac enrichment over <i>YFR057w</i> promoter and ORF was assayed.</p
