Biology subjects

Zanella, M.

Publications and source records attributed to Zanella, M..

4 recordsLinked to original sources

bioRxiv2026

qg: Configuration-Driven, Multi-Vendor Acquisition Queue Generation with Reproducible Run-Order and QC Control for Mass Spectrometry

Mass spectrometry laboratories must turn lists of submitted samples into acquisition queues. The run order and the placement of quality-control (QC) injections determine whether a design controls batch effects and signal drift, and whether those effects stay correctable afterward. Yet operators usually set them by hand in vendor worklist editors that neither randomize run order nor offer configurable, pattern-driven QC. We present qg, an open-source tool that builds acquisition queues with systematic run-order handling: four run-order modes (none, simple, blocked/randomized-complete-block, and group-uniform blocked), pattern-driven QC and standard injections, and sampler- and plate-aware positioning. Unlike plate-design tools that stop at a generic sample sheet, qg writes the native vendor acquisition file directly, for three instrument ecosystems (Thermo Fisher XCalibur, Axel Semrau Chronos, Bruker HyStar) across proteomics, metabolomics, and lipidomics. It separates a small, stateless generation pipeline from a declarative configuration layer, so a laboratory adapts instruments, QC patterns, layouts, and naming by editing version-controlled configuration through a validating editor rather than changing code. qg runs from a reactive web interface or a scripted command-line interface, integrated with a LIMS (B-Fabric) or standalone from uploaded tables; randomized runs record their seed and reproduce from exported parameters. On an unbalanced design, group-uniform blocked randomization spreads biological groups evenly across acquisition time, whereas textbook block randomization leaves a tail of the largest group and can track acquisition time worse than a plain shuffle. qg is released under the Apache-2.0 license.

bioinformatics↗

bioRxiv2025

PKA regulates stress granule maturation to allow timely recovery after prolonged starvation

Cells have evolved multiple strategies to survive environmental stress conditions. This includes the formation of membrane-less cytoplasmic ribonucleoprotein structures called stress granules (SGs) that sequester and protect mRNAs encoding many housekeeping genes. SGs are not static biomolecular condensates but transform into solid states during a maturation phase. Although SG maturation is a hallmark of many neurodegenerative pathologies, little is known about the mechanisms and physiological relevance underlying the maturation process. Here we show that yeast SGs mature into a solid-like state during long-term stationary phase stress, which delays SG disassembly and cell cycle restart. Profiling of phosphorylation sites during stationary phase revealed that SG maturation is driven by protein kinase A (PKA)-dependent phosphorylation of the SG proteome. Indeed, upon stationary phase the catalytic PKA subunits condense in SGs where they maintain kinase activity, while during this time cytoplasmic PKA is inhibited. PKA-mediated phosphorylation of key SG components, like the pyruvate kinase Cdc19, is necessary and sufficient for its timely accumulation in SGs, where Cdc19 assembles into amyloid-like structures. Importantly, inhibiting PKA during long-term stationary phase prevents SG maturation, delaying ordered re-start of cell growth after re-feeding. Taken together, these results describe a SG maturation mechanism, selectively activated during chronic stress, that preserves SG integrity and promotes cell survival. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=164 HEIGHT=200 SRC="FIGDIR/small/663161v1_ufig1.gif" ALT="Figure 1"> View larger version (25K): org.highwire.dtl.DTLVardef@19c4d82org.highwire.dtl.DTLVardef@a4cf27org.highwire.dtl.DTLVardef@1c2577org.highwire.dtl.DTLVardef@1dfe84f_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIStress granules mature during chronic stress such as long-term stationary phase C_LIO_LIPhosphorylation of SG components by PKA is a hallmark of SG maturation C_LIO_LIPhosphorylation of Cdc19 by PKA promotes its maturation into an amyloid-like state C_LIO_LISG maturation acts as a timer for recovery after chronic stress C_LI

cell biology↗

bioRxiv2019

7q11.23 Syndromes Reveal BAZ1B as a Master Regulator of the Modern Human Face and Validate the Self-Domestication Hypothesis

Symmetrical 7q11.23 dosage alterations cause craniofacial and cognitive/behavioral phenotypes that provide a privileged entry point into the evolution of the modern human face and (pro-) sociality. We undertook a functional dissection of chromatin remodeler BAZ1B in neural crest stem cells (NCSCs) from a uniquely informative cohort of typical and atypical patients harboring 7q11.23 Copy Number Variants (CNVs). Our results reveal a key contribution of BAZ1B to NCSC in vitro induction and migration, coupled with a crucial involvement in neural crest (NC)-specific transcriptional circuits and distal regulation. By intersecting our experimental data with new paleogenetic analyses comparing modern and archaic humans, we uncover a modern-specific enrichment for regulatory changes both in BAZ1B and its experimentally defined downstream targets, thereby providing the first empirical validation of the self-domestication hypothesis and positioning BAZ1B as a master regulator of the modern human face.\n\nOne Sentence SummaryBAZ1B dosage shapes the modern human face.

evolutionary biology↗

bioRxiv2017

From Cohorts to Molecules: Adverse Impacts of Endocrine Disrupting Mixtures

Convergent evidence associates endocrine disrupting chemicals (EDCs) with major, increasingly-prevalent human disorders. Regulation requires elucidation of EDC-triggered molecular events causally linked to adverse health outcomes, but two factors limit their identification. First, experiments frequently use individual chemicals, whereas real life entails simultaneous exposure to multiple EDCs. Second, population-based and experimental studies are seldom integrated. This drawback was exacerbated until recently by lack of physiopathologically meaningful human experimental systems that link epidemiological data with results from model organisms.\n\nWe developed a novel approach, integrating epidemiological with experimental evidence. Starting from 1,874 mother-child pairs we identified mixtures of chemicals, measured during early pregnancy, associated with language delay or low-birth weight in offspring. These mixtures were then tested on multiple complementary in vitro and in vivo models. We demonstrate that each EDC mixture, at levels found in pregnant women, disrupts hormone-regulated and disease-relevant gene regulatory networks at both the cellular and organismal scale.

molecular biology↗