NdpA2 & TprA regulon in PA14: ICE PAPI-1 transference induced (M0) vs Control (Tn38)
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PROVIDER: PRJNA638397 | ENA |
REPOSITORIES: ENA
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Project description:NdpA2 & TprA regulon in PA14: ICE PAPI-1 transference induced (M0) vs PAPI-1 transference inactivated (M0-59060-stop)
| PRJNA638396 | ENA
Project description:Transcriptional profiling of Pseudomonas aeruginosa PA14 comparing T4SS-GI induced biosynthesis M0 strain with control T4SS-GI induced biosynthesis M0-59060-stop strain. The PA14_59050-59120 locus was overexpressed through chromosomal insertion of ptac promoter within PA14_59030 gene.
2021-01-31 | GSE152140 | GEO
Project description:Transcriptional profiling of Pseudomonas aeruginosa PA14 comparing T4SS-GI induced biosynthesis M0 strain with control wild type phentoype Tn38 strain The PA14_59050-59120 locus was overexpressed through chromosomal insertion of ptac promoter within PA14_59030 gene.
2021-01-31 | GSE152141 | GEO
Project description:Bombyx Papi contains two K-homology (KH) domains and one Tudor domain, and acts as a scaffold for Siwi-piRISC biogenesis on the mitochondrial surface. To initiate this process, Papi binds first to Siwi via the Tudor domain and subsequently to piRNA precursors loaded onto Siwi via the KH domains. This second action depends on phosphorylation of Papi. However, its underlying mechanism remains unknown. Here, we show that Siwi targets Par-1 kinase to mitochondrial Papi to promote its phosphorylation at Ser547 in the auxiliary domain and that this modification enhances the ability of Papi to bind Siwi-bound piRNA precursors via the KH domains. Papi S547A mutant still bound to Siwi, like wild-type (WT) Papi, although it evaded phosphorylation by Par-1: Consequently, Papi lost the ability to bind RNAs, abrogating the generation of Siwi-piRISC. Papi mutant lacking the Tudor and auxiliary domains escaped coordinated regulation by Siwi and Par-1 and lost their bias to bind piRNA precursors. Pseudo-phosphorylation mutants of Papi restored Siwi-piRISC formation in Papi-lacking cells, but their ability to bind RNAs required Siwi, similar to WT Papi. Par-1-dependent, multilayered mechanism by which Siwi regulates the role of Papi in Siwi-piRISC biogenesis was revealed.
2022-01-25 | GSE179432 | GEO
Project description:PIWI-interacting RNAs (piRNAs) are germline-enriched small RNAs that control transposons to maintain genome integrity1,2,3. To achieve this, piRNAs bind PIWI proteins upon being processed from piRNA precursors1,2,3. Bioinformatic studies of piRNA biogenesis in Drosophila showed that the piRNA 5′ end is formed by PIWI-Slicer or Zucchini (Zuc) endonucleolytic cleavage, while the 3′ end is formed by Zuc or Nibbler (Nbr) 3′-to-5′ exonucleolytic activity4,5,6. piRNA 3′-end formation in Bombyx was shown to be mediated by PNLDC1/Trimmer (Trim) 3′-to-5′ exonuclease7, while piRNA intermediates are bound with PIWI anchored onto mitochondrial protein PAPI8. However, the requirement for Zuc and Nbr in piRNA biogenesis in Bombyx has not been elucidated. Here, we applied biochemical approaches to understand their involvement in piRNA biogenesis and revealed that Zuc endonuclease, but not Trim and Nbr exonucleases, plays a crucial role in Bombyx piRNA 3′-end formation. Loss of Zuc had little effect on the levels of Trim and Nbr, but led to the aberrant accumulation of piRNA intermediates within the PAPI complex, which were processed to mature piRNAs by recombinant Zuc. Zuc copurified with PAPI, and PAPI exerted RNA-binding activity only when Siwi coexisted with it and PAPI was phosphorylated, suggesting that complex assembly proceeds via a hierarchical process. Bioinformatic analyses of piRNA intermediates within the PAPI complex revealed that both the 5′ and the 3′ ends showed the hallmark of PIWI-Slicer, yet no phasing pattern was observed in mature piRNAs. These findings strongly support the notion that, in Bombyx piRNA, the 5′ end is formed by PIWI-Slicer, but independently of Zuc, while the 3′ end is formed by Zuc endonuclease. The Bombyx piRNA biogenesis is simpler than that of Drosophila, which is reasonable considering that Bombyx has no transcriptional silencing machinery relying on phased piRNAs.
2018-03-01 | GSE107371 | GEO
Project description:PA3225 is a LysR-type transcriptional regulator, and the ΔPA3225 deletion mutant is more resistant to various antibiotics than the wild-type PA14 strain in both planktonic and biofilm cells. In order to characterise the regulon of PA3225, we compared the transcriptomes of biofilm and planktonic ΔPA3225 to biofilm and planktonic PA14 wild-type by RNA-seq.
2017-06-08 | GSE87213 | GEO
Project description:Pseudomonas aeruginosa is a major cause of nosocomial infections, particularly in immunocompromised patients or in individuals with cystic fibrosis. Genome sequences reveal that most P. aeruginosa strains contain a significant number of accessory genes gathered in genomic islands. Those genes are essential for P. aeruginosa to invade new ecological niches with high levels of antibiotic usage, like hospitals, or to survive during host infection by providing pathogenicity determinants. P. aeruginosa pathogenicity island 1 (PAPI-1), one of the largest genomic islands, encodes several putative virulence factors, including toxins, biofilm genes and antibiotic-resistance traits. The integrative and conjugative element (ICE) PAPI-1 is horizontally transferable by conjugation via a specialized GI-T4SS, but the mechanism regulating this transfer is currently unknown. Here, we show that this GI-T4SS conjugative machinery is directly induced by TprA, a regulator encoded within PAPI-1. Our data indicate that the nucleotide associated protein NdpA2 acts in synergy with TprA, removing a repressive mechanism exerted by MvaT. In addition, using a transcriptomic approach, we unravelled the regulon controlled by Ndpa2/TprA and showed that they act as major regulators on the genes belonging to PAPI-1. Moreover, TprA and NdpA2 trigger an atypical biofilm structure and enhance ICE PAPI-1 transfer.
| S-EPMC8565334 | biostudies-literature
Project description:Pseudomonas aeruginosa PA14 isolate:PA14 Genome sequencing
| PRJNA1028549 | ENA
Project description:Pseudomonas aeruginosa is a leading cause of hospital-acquired pneumonia and severe chronic lung infections in cystic fibrosis patients. The reference strains PA14 and PAO1 have been studied extensively, revealing that PA14 is more virulent than PAO1 in diverse infection models. Among other factors, this may be due to two pathogenicity islands, PAPI-1 and PAPI-2, both present in PA14 but not in PAO1. We compared the global contributions to virulence of PAPI-1 and PAPI-2, rather than that of individual island-borne genes, using murine models of acute pneumonia and bacteremia. Three isogenic island-minus mutants (PAPI-1-minus, PAPI-2-minus, and PAPI-1-minus, PAPI-2-minus mutants) were compared with the wild-type parent strain PA14 and with PAO1. Our results showed that both islands contributed significantly to the virulence of PA14 in acute pneumonia and bacteremia models. However, in contrast to the results for the bacteremia model, where each island was found to contribute individually, loss of the 108-kb PAPI-1 island alone was insufficient to measurably attenuate the mutant in the acute pneumonia model. Nevertheless, the double mutant was substantially more attenuated, and exhibited a lesser degree of virulence, than even PAO1 in the acute pneumonia model. In particular, its ability to disseminate from the lungs to the bloodstream was markedly inhibited. We conclude that both PAPI-1 and PAPI-2 contribute directly and synergistically in a major way to the virulence of PA14, and we suggest that analysis of island-minus strains may be a more appropriate way than individual gene knockouts to assess the contributions to virulence of large, horizontally acquired segments of DNA.
| S-EPMC2849418 | biostudies-literature
Project description:Ficolled AML-M0 sample gene expression profiles on Affymetrix HGU133Plus2.0 GeneChips. Acute myeloid leukemia (AML) classified as FAB-M0 is defined as a subtype with minimally differentiated morphology. Here we investigated by gene expression (GEP) profiling whether AML-M0 cases should be considered as one or more unique molecular subgroups that discriminates them from other AML patients. By applying GEP and subsequent unsupervised analysis of 35 AML-M0 samples and 253 previously reported AML cases, we demonstrate that AML-M0 cases express a unique signature. Hematological transcription regulators such as CEBPA, CEBPD, PU.1 and ETV6 and the differentiation associated gene MPO appeared strongly down-regulated, in line with the very primitive state of this type of leukemia. Moreover, AML M0 cases appeared to have a strong positive correlation with a previously defined immature AML subgroup with adverse prognosis. AML-M0 leukemias frequently carry loss-of-function RUNX-1 mutation and unsupervised analyses revealed a striking distinction between cases with and without mutations. RUNX1 mutant AML-M0 samples showed a distinct up-regulation of B-cell-related genes, e.g. members of the B-cell receptor complex, transcriptions regulators RUNX3, ETS2, IRF8 or PRDM1 and major histocompatibility complex class II genes. Importantly, expression of one single gene, i.e. BLNK, enabled prediction of RUNX1 mutations in AML-M0 with high accuracy. We propose that RUNX1 mutations in this subgroup of AML cause lineage infidelity, leading to aberrant co-expression of myeloid and B-lymphoid genes in the same cells. Experiment Overall Design: 35 samples
2009-07-18 | E-GEOD-17061 | biostudies-arrayexpress