MicroRNA-128-2 targets the transcriptional repressor E2F5 enhancing mutant p53 gain of function
Sara DonzelliGiulia FontemaggiFrancesco FaziSilvia Di AgostinoFabrizio PadulaFrancesca BiagioniPaola MutiSabrina StranoGiovanni Blandino
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We have isolated a novel enhanced-nodulating mutant astray (Ljsym77) from Lotus japonicus. The name astray derives from the non-symbiotic phenotype of this mutant, agravitropic lateral roots that go “astray” against gravity. In this report we evaluated the symbiotic aspects of this mutant in detail. The astray mutant developed approximately twice the number of nodules on a wider area of roots compared with the wild type. Furthermore, the astray mutant demonstrated early initiation of nodule development, which is an unprecedented symbiotic phenotype. The astray seedlings showed normal sensitivity to the general inhibitors of nodulation such as ethylene and nitrate. These results indicate that the astray mutant is distinct from the hypernodulating mutants reported previously, and that the ASTRAY gene acts as an early and negative regulator in the cascade of nodule development.
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To investigate the architecture of the rolled leaf morphology in rice,the features of phenotype and histological level in 2 reverse rolled leaf mutants derived from rice Ac/Ds transposons insertional mutant library were investingated. The results showed that the number of bulliform cells was reduced in 2 reverse rolled leaf mutants(Ad-mutant:adaxial rolled mutant;Ab-mutant:abaxial rolled mutant) compared with the normal flat leaf in wild type,which may be an important cause of the rolled leaf in rice. And the number of parenchyma also was reduced and dehisced to 2 large air cavities in Abmutant. The cellulose content of leaf and culm in 2 rolled leaf mutant and wild type was measured,and the result showed that the cellulose content of leaf and culm in Ab-mutant was significant reduced compared with Ad-mutant and wild type.But the cellulose content of leaf and culm in Ad-mutant was not significantly different from that of wild type. This result suggested that Ab-mutant and Ad-mutant may be different in mutation of gene loci. In addition,the genetic rule of Abmutant and Ad-mutant was analyzed,and the result showed that both of them were controlled by single recessive gene.
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Direct measurements of the intracellular level of λ repressor have been made by a DNA-filter assay and a radioimmune assay. Transcription of cI , the structural gene for repressor, appears to initiate at two different promoters, prm and pre . Promoter pre is activated during the establishment of lysogeny by the action of cII and cIII proteins at the DNA site cY . Phage mutated in cII, cIII , or cY do not make a normal burst of repressor after infection and do not efficiently lysogenize the cell. Cro product stops repressor synthesis midway in the infective cycle. Promoter prm maintains the repressor level in established lysogens. Delection mapping places it very near the right operator ( Or ). Prm is activated by repressor bound to the right operator. In the absence of cII or cIII protein, repressor synthesis requires active repressor and only proceeds on genomes able to bind repressor at Or .
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MicroRNAs (miRNAs) are ∼22 nt long, non‐coding RNAs that guide post‐transcriptional gene silencing of their target genes and regulate diverse biological processes including cancer. miRNAs do not act alone, but require assembly into RNA‐induced silencing complex (RISC). In this review, we summarize how miRNAs are produced, assembled into RISC, and regulate target mRNAs, and discuss how the miRNA pathway is involved in cancer. ( Cancer Sci 2010; 101: 2309–2315)
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SUMMARY: An investigation was undertaken to determine to what extent the properties of oligosporogenous (Osp) mutants allow them to be considered as a separate class of sporulation mutant, distinct from asporogenous (Sp-) mutants. Of thirty Osp mutants examined, seventeen at least had a phenotype which had previously been identified with a Sp- mutant. The majority of cells in an Osp culture either reached a particular stage in the sporulation process and then stopped, or in some cases went on to produce aberrant forms. Some of these aberrant forms have their counterparts in Sp- mutants described by other authors, but some present new features. The morphological and biochemical sequences were linked so that if the majority of cells were blocked at a certain stage, then the biochemical sequence stopped accordingly. The general similarity in behaviour between the two types of mutant is consistent with the assumption that at least some of the Osp mutants have leaky mutations in genes where mutation can also give rise to Sp- phenotypes. Evidence is presented to suggest that the ability of a cell of an Osp mutant to overcome its block, and so go on to form a spore, is a chance event when that stage in the process is reached. A mutant has been obtained in which the spores are octanol-resistant yet contain no measurable dipicolinate. In several other mutants the spores contained well-developed coat layers, but the cortex was poorly formed or completely missing.
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The λ phage repressor binds cooperatively to the three sites in the right operator ( O R ) according to the following pattern. If the DNA is wild type, O R 1 and O R 2 are filled coordinately because of interactions between repressor dimers bound to these two sites. Site O R 3 is filled only at higher repressor concentrations. In contrast, if O R 1 is mutant, O R 2 and O R 3 are filled coordinately because of interactions between repressors bound to these sites. In this case, the affinity of O R 3 is increased and that of O R 2 is decreased relative to the wild type. We infer that a repressor dimer bound to the middle site O R 2 can interact either with another repressor dimer bound to O R 1 (wild-type case) or, alternatively, with one bound to O R 3 (mutant O R 1 case). We argue that these repressor interactions are mediated by protein-protein contacts between adjacent repressor dimers, because the isolated amino-terminal domains of repressor bind to the operator sites noncooperatively. The cro protein of phage λ, a second regulatory protein, which recognizes the same three sites in O R as does repressor, binds non-cooperatively. Experiments performed in vivo show that regulation of gene expression by repressor can be influenced critically by cooperative interactions. We demonstrate that the effect of repressor in a lysogen on the activity of the promoter P RM can be changed from activation to repression by deletion of O R 1. We explain this effect in terms of the alternative cooperative interactions described above.
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