Biology subjects

Teuliere, J.

Publications and source records attributed to Teuliere, J..

4 recordsLinked to original sources

bioRxiv2026

GenDiMug: a generic inclusive multigraph framework to analyze genomic organizations and -omics data at multiple scales

After decades of investigation, analyses of genome organization remain challenging. This is because genome descriptions are very information-rich and usually rendered as a linear map of genomic features corresponding to an ordered list of position intervals on a nucleic acid macromolecular backbone. This formalism, while accurate, is not fully optimized to mathematically analyze all genome structural properties, in particular the relations between genomic features, nor to integrate large amounts of -omics data, such as transcriptomes, epigenomes, proteomes, meltomes or chromatin accessibility data, which are increasingly available. We therefore developed GenDiMug, a tool that uses a network representation of the genome as a backbone, providing a natural framework to integrate spatial and ontogenetic relationships between genomic features and multi-omics data. We illustrate how this generic approach can be applied to all sorts of genomes, both to visualize genomic topology at contig and chromosomal scales at base-pair resolution, and to analyze genome positional effects using various graph metrics. Using GenDiMug, we further reveal clumping of genes with similar expression levels in eukaryotic genomes and their possible circadian regulation in a photosynthetic alga.

bioinformatics↗

bioRxiv2024

Transcriptional landscape of the archaeal cell cycle is broadly conserved in eukaryotes

The cell cycle is a series of events that occur from the moment of cell birth to cell division. In eukaryotes, cell growth, genome replication, genome segregation, and cytokinesis are strictly coordinated, defining discrete cell cycle phases. In contrast, these key processes may occur concurrently in bacteria. Thermoacidophilic archaea in the genus Saccharolobus follow a defined cell cycle program, with the first pre-replicative growth (G1) phase, followed by the chromosome replication (S) phase, the second growth (G2) phase, and rapid genome segregation (M) and cytokinesis (D) phases. However, whether other processes, such as metabolism, catabolism, protein translation, and antiviral defense also occur at specific cell cycle phases, as in eukaryotes, or are active throughout the cell cycle, as in bacteria, remains unclear. To address this question, we synchronized cultures of S. islandicus and performed an in-depth transcriptomic analysis of samples enriched in cells undergoing the M-G1, S, and G2 phases. Differential gene expression and consensus gene co-expression network analyses provided a holistic view of the S. islandicus cell cycle. In addition to the core transcriptome network, which is expressed throughout the cell cycle, we show that diverse metabolic pathways, protein synthesis, cell motility and even antiviral defense systems, are expressed in a cell cycle dependent fashion. Our data also refines understanding of the processes previously known to be linked to the cell cycle, such as DNA replication. We show that most DNA replication genes are expressed prior to the S phase, during the M-G1, whereas expression of the major chromatin genes, and accordingly, chromatinization are concomitant with replication. A statistical model was used to define sets of signature genes characteristic of each of the analyzed cell cycle phases, emphasizing transcriptional stratification of the phases. Signature genes are more conserved across Thermoproteota than non-signature genes and their peak expression, especially for the M-G1 and G2 specific genes, matches that of homologs in yeast. Collectively, our data elucidate the complexity of the S. islandicus cell cycle and suggest that it more closely resembles the cell cycle of eukaryotes than previously appreciated.

microbiology↗

bioRxiv2022

NMY-2, TOE-2 and PIG-1 Regulate C. elegans Asymmetric Cell Divisions

Asymmetric cell division (ACD) is an important mechanism that generates cellular diversity during development. Not only do asymmetric cell divisions produce daughter cells of different fates, many can produce daughters of different sizes, which we refer to as Daughter Cell Size Asymmetry (DCSA). In C. elegans, apoptotic cells are frequently produced by asymmetric divisions that exhibit DCSA, where the smaller daughter dies. We focus here on the divisions of the Q.a and Q.p neuroblasts, which produce apoptotic cells and divide with opposite polarity using both distinct and overlapping mechanisms. The PIG-1/MELK and TOE-2 proteins both regulate DCSA and specify the apoptotic cell fate in both the Q.a and Q.p divisions. In many asymmetric cell divisions, the non-muscle myosin NMY-2 is involved in properly positioning the cleavage furrow to produce daughters of unequal size. It was previously reported that NMY-2 is asymmetrically distributed and required for the DCSA of Q.a but not Q.p. In this study, we examined endogenously tagged reporters of NMY-2, TOE-2, and PIG-1 and found that all were asymmetric at the cortex during both the Q.a and Q.p divisions. TOE-2 and NMY-2 were biased toward the side of the dividing cell that would produce the smaller daughter, whereas PIG-1 was biased toward the side that would produce the larger daughter. We used temperature-sensitive nmy-2 mutants to determine the role of nmy-2 in these divisions and found that these mutants only displayed DCSA defects in the Q.p division. We generated double mutant combinations between the nmy-2 mutations and mutations in toe-2 and pig-1. The nmy-2 mutations did not significantly alter the DCSA of the toe-2 and pig-1 mutants but did alter the fate of the Q.a and Q.p daughters. This finding suggests that NMY-2 functions together with TOE-2 and PIG-1 to regulate DCSA but plays an independent role in specifying the fate of the Q.a and Q.p descendants.

genetics↗

bioRxiv2018

The Caenorhabditis elegans HAM-1 protein modifies G protein signaling and membrane extension to reverse the polarity of asymmetric cell division

Asymmetric divisions often produce daughter cells that differ in both fate and size. The Caenorhabditis elegans HAM-1 protein regulates both daughter cell fate and daughter cell size asymmetry (DCSA) in a subset of asymmetric divisions. Here we focus on the divisions of the Q.a and Q.p neuroblasts, which use distinct mechanisms to divide with opposite polarity. Q.a divides by a ham-1-dependent, spindle-independent, myosin-dependent mechanism to produce a smaller anterior daughter that dies, whereas Q.p divides by a ham-1-independent, spindle-dependent, myosin-independent mechanism to produce a smaller posterior daughter that dies. Despite these differences, we found that membrane extension at the posterior of Q.a and at the anterior of Q.p promoted DCSA in these cells by a Wiscott-Aldrich protein (WASp)-dependent mechanism and that in ham-1 mutant Q.a divisions, the polarity of this extension was reversed. In addition, the spindle moved posteriorly during the Q.a division in a ham-1 mutant, a phenotype normally exhibited by Q.p. We found that this spindle movement in wild-type Q.p divisions required Ga proteins that promote spindle movement in other asymmetric divisions, and GPR-1, a protein involved in linking G proteins to microtubule asters, localized to the posterior cortex of Q.p. Genetic interactions suggest that ham-1 mutant Q.a divisions also require Ga proteins function to divide with a reversed polarity. The transformation of Q.a to Q.p-like polarity in the ham-1 mutant, however, appeared incomplete: ham-1 loss did not alter the asymmetric localization of the non-muscle myosin NMY-2 to the anterior cortex of Q.a. A GFP tagged ham-1 transgene revealed that Q.a but not Q.p expressed ham-1. Finally, we show that HAM-1 has both cortical and nuclear functions in Q,a DCSA. We propose a model where HAM-1 modifies a default Q.p-type polarity by localizing WASp function to the posterior Q.a membrane and by interfering with G-protein mediated spindle movement.\n\nAuthor SummaryOne way that animals produce different cell types is by asymmetric cell division, where a cell divides to produce daughter cells that differ in fate. Much is known about the mechanisms that polarize dividing cells to generate daughters that differ in fate. Some asymmetric cell divisions also result in daughters that differ in size, and the mechanisms that regulate how cells generate an asymmetric cleavage plane are poorly understood. In neural progenitors of the nematode Caenorhabditis elegans, two distinct mechanisms generate daughter cells of different size. One type requires movement of the mitotic spindle, which then defines the plane of the cell division. The other is spindle-independent. Here, we study two cells that divide with opposite polarities using these two mechanisms. We find that in the absence of the protein HAM-1, which has been reported to regulate gene transcription, the cell that normally divides using a spindle-independent mechanism now divides with a reversed polarity using a spindle-dependent mechanism. Our findings suggest that HAM-1 plays a key role in defining the mechanism by which a progenitor divides to produce daughter cells of different sizes and that both localization to the cell periphery and nucleus are important for its function.

developmental biology↗