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Froment, C.

Publications and source records attributed to Froment, C..

9 recordsLinked to original sources

Bacterial persistence emerges mainly from antibiotic-specific networks rather than slow growth

Bacterial persisters are rare phenotypic variants that survive antibiotic treatment and contribute to infection relapse and resistance emergence, yet the genetic basis of persistence remains only partially understood. Here, we developed a genome-wide Tn-seq approach to identify genes and pathways involved in persistence in exponentially growing Escherichia coli while avoiding persister enrichment and controlling for the confounding effects of growth. We found that persistence was largely independent of growth, and mutations that impaired growth could either increase or decrease survival. Furthermore, persistence was strongly antibiotic-specific. Ampicillin persistence relied primarily on pathways linked to energy metabolism, whereas ofloxacin persistence was associated on pathways involved in DNA repair and the maintenance of genome integrity. This study supports a model in which bacterial persistence is mainly an antibiotic-specific phenomenon governed by distinct physiological pathways rather than being universally associated with growth arrest.

microbiology↗

Translatome and translation dynamics analysis of a RiboCancer cell line panel reveals that leukemia-associated Rps15 mutations rewire translation through codon-specific tRNA accommodation defects.

Deletions and point mutations targeting ribosomal proteins (RPs) have been identified in cancer. Yet, their role in translational dysregulation remains poorly understood. We performed an integrated genome-wide translatome analysis (proteome, Ribo-seq and total RNA-seq) as well as RiboMethSeq on an isogenic cell line library modeling the most recurrent RP defects in cancer (Rpl5+/-, Rpl11+/-, Rpl22+/-, Rpl22-/-, Rpl10 R98S, Rps15 P131S and Rps15 H137Y). RP knock-out had minimal effects on translation, whereas RP point mutations induced a significant number of translation efficiency changes, affecting up to 10% of expressed genes in Rps15 mutants associated with Chronic Lymphocytic Leukemia (CLL). Cryo-electron microscopy and biochemical analyses revealed that the Rps15 mutations destabilize the C-terminal Rps15 domain, affecting the translation elongation cycle dynamics, and deregulating accommodation of aminoacylated tRNAs at the ribosomal A-site. Using Ribo-seq and translation reporter assays, we show that this accommodation defect shows codon specificity, explaining the reduced translation efficiency of genes enriched for these codons in Rps15 mutant cells, such as histones. Notably, genes with reduced translation efficiency in Rps15 mutated cells were enriched for transcriptional regulators such as transcription factor Runx3, resulting in downregulation of Runx3 target genes involved in immune regulation. Altogether, this study provides a comparative map of the translational rewiring driven by the most frequent somatic RP mutations. We provide unprecedented mechanistic insights in the translation defects induced by CLL-associated Rps15 mutations, and reveal an unappreciated cross-talk between translational and transcriptional dysregulation in these RP mutant cells. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=102 SRC="FIGDIR/small/687986v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@cd2846org.highwire.dtl.DTLVardef@10f3c49org.highwire.dtl.DTLVardef@13f1595org.highwire.dtl.DTLVardef@a212df_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

Structural Basis of Lipopolysaccharide Assembly by the Outer Membrane Translocon Holo-Complex

Lipopolysaccharide (LPS) assembly at the surfaces-exposed leaflet of the bacterial outer membrane (OM) is mediated by the OM LPS translocon. An essential transmembrane {beta}-barrel protein, LptD, and a cognate lipoprotein, LptE, translocate LPS selectively into the OM external leaflet via a poorly understood mechanism. Here, we characterize two additional translocon subunits, the lipoproteins LptM and LptY (formerly YedD). We use single-particle cryo-EM analysis, functional assays and molecular dynamics simulations to visualize the roles of LptM and LptY at the translocon holo-complex LptDEMY, uncovering their impact on LptD conformational dynamics. Whereas LptY binds and stabilizes the periplasmic LptD {beta}-taco domain that functions as LPS receptor, LptM intercalates the lateral gate of the {beta}-barrel domain, promoting its opening and access by LPS. Remarkably, we demonstrate a conformational switch of the LptD {beta}-taco/{beta}-barrel interface alternating between contracted and extended states. The LptD {beta}-strand 1, which defines the mobile side of the lateral gate, binds LPS and performs a stroke movement toward the external leaflet during the contracted-to-extended state transition. Our findings establish a detailed mechanistic framework explaining the selective transport of LPS to the membrane external leaflet.

microbiology↗

Fibrillarin-mediated ribosomal RNA maturation is a novel therapeutic vulnerability in triple-negative breast cancer

Triple-negative breast cancer (TNBC) remains one of the most challenging breast cancer subtypes to treat due to the lack of effective therapeutic options. Ribosome biogenesis has recently emerged as a promising therapeutic target across various cancers. Despite the current targeting of ribosome biogenesis through RNA polymerase I (RNA Pol I) inhibition, we speculated that other factors essential for ribosome assembly, such as rRNA maturation factors, may also represent therapeutic targets in TNBC. Here, we demonstrate that ribosome biogenesis-related genes are notably overexpressed in TNBC compared to other breast cancer subtypes, highlighting its critical role in TNBC progression. Accordingly, we show that RNA Pol I inhibition exerts potent anti-proliferative effects in pre-clinical models of TNBC, both in vitro and in vivo. However, the DNA-damaging activity of RNA Pol I inhibitors raises safety concerns, highlighting the need for alternative strategies to inhibit ribosome biogenesis. To this end, we show that targeting a downstream rRNA maturation step, specifically pre-rRNA cleavage, by inhibiting the maturation factor Fibrillarin, also inhibits tumor growth in TNBC models. Notably, ribosome biogenesis inhibition, through either RNA Pol I or Fibrillarin targeting, induces cell cycle arrest without triggering significant cell death. These findings establish ribosome biogenesis as a therapeutic vulnerability in TNBC and identify rRNA maturation, and Fibrillarin in particular, as novel targets for potential therapeutic intervention. SignificanceTargeting ribosome biogenesis, through inhibition of either rRNA synthesis or maturation, induces anti-tumoral effects in TNBC, representing a novel therapeutic vulnerability with potential to improve patient outcomes.

cancer biology↗

SURF2 is a MDM2 antagonist in triggering the nucleolar stress response

Cancer cells are addicted to strong ribosome production to sustain their proliferation rate. Many chemotherapies impede ribosome production which is perceived by cells as "nucleolar stress" (NS), triggering p53-dependent and independent response pathways leading to cell cycle arrest and/or apoptosis. The 5S RNP particle, a sub-ribosomal particle, is instrumental to NS response. Upon ribosome assembly defects, the 5S RNP accumulate as free form. This free form is able to sequester and inhibit MDM2, thus promoting p53 stabilization. To investigate how cancer cells can resist to NS, we purified free-5S RNP and uncovered a new interaction partner, SURF2. Functional characterization of SURF2 shows that its depletion increases cellular sensitivity to NS, while its overexpression promotes their resistance to it. Consistently, SURF2 expression level negatively correlates with the overall survival in adrenocortical and head and neck squamous cell carcinomas. Our data demonstrate that SURF2 buffers free-5S RNP particles, and can modulate their activity. SURF2 regulates NS responses, and is a key player in both ribosomopathies and oncogenic mechanisms.

cell biology↗

LptM promotes oxidative maturation of the lipopolysaccharide translocon by substrate binding mimicry.

Insertion of lipopolysaccharide (LPS) into the outer membrane (OM) of Gram-negative bacteria is mediated by a druggable OM translocon consisting of a {beta}-barrel membrane protein, LptD, and a lipoprotein, LptE. The {beta}-barrel assembly machinery (BAM) assembles LptD together with LptE to form a plug-and-barrel structure. In the enterobacterium Escherichia coli, formation of two native disulfide bonds in LptD controls LPS translocon activation. Here we report the discovery of LptM (formerly YifL), a conserved lipoprotein that assembles together with LptD and LptE at the BAM complex. We demonstrate that LptM stabilizes a conformation of LptD that can efficiently acquire native disulfide bonds and be released as mature LPS translocon by the BAM complex. Inactivation of LptM causes the accumulation of non-natively oxidized LptD, making disulfide bond isomerization by DsbC become essential for viability. Our structural prediction and biochemical analyses indicate that LptM binds to sites in both LptD and LptE that are proposed to coordinate LPS insertion into the OM. These results suggest that LptM facilitates oxidative maturation of LptD by mimicking LPS binding, thereby activating the LPS translocon.

microbiology↗

Attachment of the RNA degradosome to the inner cytoplasmic membrane of Escherichia coli prevents wasteful degradation of rRNA intermediates in ribosome assembly.

BackgroundRNase E has crucial roles in the initiation of mRNA degradation, the processing of stable transcripts such as rRNA and tRNA, and the quality control of ribosomes. With over 20000 potential cleavage sites, RNase E is a low specificity endoribonuclease with the capacity to cleave multiple times nearly every transcript in the cell. A large noncatalytic region in the C-terminal half of RNase E is the scaffold for assembly of the multienzyme RNA degradosome. The components of the RNA degradosome cooperate in the degradation of mRNA to oligoribonucleotides, which are then degraded to nucleotides by oligoribonuclease. Over the past decade, compelling evidence has emerged that the RNA degradosome is attached to the phospholipid bilayer of the inner cytoplasmic membrane by the Membrane Targeting Sequence (MTS), which is a 15-residue amphipathic alpha-helix located in the noncatalytic region of RNase E. Systematic proteomic analyses have identified RNase E as an inner membrane protein that can only be solubilized by disrupting the phospholipid bilayer with detergent. Important components of the mRNA degradation machinery are therefore membrane-attached. The reason for this cellular localization has until now been a mystery. ResultsWe have constructed and characterized the rne{Delta}MTS strain expressing ncRNase E (nucleo-cytoplasmic-RNase E), which is a soluble variant that is uniformly distributed in the interior of the cell. In the mutant strain, there is a slowdown in the rates of growth and mRNA degradation. Surprisingly, we have identified aberrant 20S and 40S ribosomal particles in the rne{Delta}MTS strain that contain, respectively, precursors of 16S and 23S rRNA that have been nicked by ncRNase E. Although intact ribosomes are resistant to RNase E cleavage in vitro, protein-free rRNA is readily degraded by RNase E. Partially unfolded ribosomes are susceptible to nicking by RNase E in vitro. We have mapped rRNA cleavage sites cRACE. In vivo and in vitro rRNA cleavages map to the same sites. The sequence of the cleavage sites matches the RNase E consensus sequence previously determined in a transcriptomic analysis that did not include rRNA. Construction of additional mutant strains demonstrated in vivo that fragments of 16S and 23S rRNA as well as a precursor of 5S rRNA are degraded in a pathway involving 3 oligoadenylation and exonucleolytic digestion. A proteomic analysis showed that 17 small subunit proteins and 21 large subunit proteins are underrepresented in the 20S and 40S particles, respectively. ConclusionsRibosome biogenesis is a complex process involving co-transcriptional rRNA folding and r-protein binding in the nucleoid. Ribonucleoprotein intermediates are released from chromatin by RNase III cleavage. Maturation continues with the addition of late proteins resulting in the compact rRNA structures found in mature 30S and 50S ribosomal subunits. Considering our experimental results, we propose that the physical separation of rRNA transcription in the nucleoid from the RNA degradosome on the inner cytoplasmic membrane protects intermediates in ribosome assembly from degradation. A corollary is that ribosome quality control normally occurs when defective ribosomal particles interact with the membrane-attached RNA degradosome. The rRNA degradation pathway described here is the same as described previously for RNase E-dependent degradation of mRNA. Since the pathway for rRNA degradation is the same as the pathway for mRNA degradation, the slowdown of mRNA degradation in the rne{Delta}MTS strain could be due to competition by rRNA degradation. Since growth rate is limited by ribosome synthesis rate, the slow growth of the rne{Delta}MTS strain is likely due to wasteful degradation of a proportion of newly synthesized rRNA. If r-proteins released by rRNA degradation are not recycled, then this would be an additional burden on cell growth. Avoiding a futile cycle in which rRNA intermediates in ribosome assembly are degraded likely explains why localization of RNase E homologues to the inner cytoplasmic membrane is conserved throughout the {beta}- and {gamma}-Proteobacteria. ImportanceIn E. coli, transcription in the nucleoid, translation in the cytoplasm and initiation of mRNA degradation on the inner cytoplasmic membrane are physically separated. Despite the lack of internal membranes, this separation can be viewed as a compartmentalization of the bacterial cell. Our work shows that the inner membrane localization of the RNA degradosome restricts access of RNase E to intermediates in ribosome assembly. Thus, as in the eukaryotic cell, the architecture of the bacterial cell has an important role in the organization of cellular processes such as ribosome biogenesis, ribosome quality control, and mRNA degradation.

molecular biology↗

Long non-coding RNA Neat1 is a key translational regulator in hypoxia.

Internal ribosome entry sites (IRESs) drive translation initiation during stress. In response to hypoxia, (lymph)angiogenic factors responsible for tissue revascularization in ischemic diseases are induced by the IRES-dependent mechanism. Here we searched for IRES trans-acting factors (ITAFs) active in early hypoxia in mouse cardiomyocytes. Using knock-down and proteomics approaches, we show a link between a stressed-induced nuclear body, the paraspeckle, and IRES-dependent translation. Furthermore, smiFISH experiments demonstrate the recruitment of IRES-containing mRNA into paraspeckle during hypoxia. Our data reveal that the long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator, active on IRESs of (lymph)angiogenic and cardioprotective factor mRNAs. In addition, paraspeckle proteins p54nrb and PSPC1 as well as nucleolin and Rps2, two p54nrb-interacting proteins identified by mass spectrometry, are ITAFs for IRES subgroups. Paraspeckle thus appears as a platform to recruit IRES-containing mRNAs and possibly host IRESome assembly. Polysome PCR array shows that Neat1 isoforms regulate IRES-dependent translation and, more widely, translation of mRNAs involved in stress response. HighlightsO_LIParaspeckle formation correlates with activation of translation via internal ribosome entry sites (IRES) in mouse hypoxic cardiomyocytes as well as in tumoral cells. C_LIO_LIThe long non-coding RNA Neat1, an essential paraspeckle component, is a key translational regulator of (lymph)angiogenic and cardioprotective factor expression in this process. C_LIO_LIIRES-containing mRNA is recruited into paraspeckles during hypoxia. C_LIO_LIParaspeckle proteins p54nrb and PSPC1 as well as two p54nrb-interacting proteins, nucleolin and RPS2, contribute to this process. C_LIO_LIParaspeckle appears as a platform for IRESome formation in the nucleus. C_LIO_LIThe Neat1 isoforms widely regulate the translation of mRNAs containing IRESs and of genes involved in the stress response. C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/430272v2_ufig1.gif" ALT="Figure 1"> View larger version (98K): org.highwire.dtl.DTLVardef@1741648org.highwire.dtl.DTLVardef@62e741org.highwire.dtl.DTLVardef@13c86a8org.highwire.dtl.DTLVardef@acae63_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

RIOK2 phosphorylation by RSK promotes synthesis of the human small ribosomal subunit

Ribosome biogenesis lies at the nexus of various signaling pathways coordinating protein synthesis with cell growth and proliferation. This process is regulated by well-described transcriptional mechanisms, but a growing body of evidence indicates that other levels of regulation exist. Here we show that the Ras/mitogen-activated protein kinase (MAPK) pathway stimulates post-transcriptional stages of human ribosome synthesis. We identify RIOK2, a pre-40S particle assembly factor, as a new target of the MAPK-activated kinase RSK. RIOK2 phosphorylation by RSK promotes cytoplasmic maturation of late pre-40S particles, which is required for optimal protein synthesis and cell proliferation. RIOK2 phosphorylation facilitates its release from pre-40S particles and its nuclear re-import, prior to completion of small ribosomal subunits. Our results bring a detailed mechanistic link between the Ras/MAPK pathway and the maturation of human pre-40S particles, which open a hitherto poorly explored area of ribosome biogenesis.

molecular biology↗