bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2020.05.12.091322

Combined pigment and metatranscriptomic analysis reveals synchronized diel patterns of phenotypic light response across domains in the open ocean

Becker, K. W.·Harke, M. J.·Mende, D. R.·Muratore, D.·Weitz, J. S.·DeLong, E. F.·Dyhrman, S. T.·Van Mooy, B. A. S.
View original source ↗Export metadata ↓

Abstract

Sunlight is the most important environmental control on diel fluctuations in phytoplankton activity, and understanding diel microbial processes is essential to the study of oceanic biogeochemical cycles. Yet, little is known about the in situ frequency of phytoplankton metabolic activities and their coordination across different populations. We investigated the diel orchestration of phytoplankton activity involved in photosynthesis, photoacclimation, and photoprotection by analyzing the pigment and quinone distribution in combination with metatranscriptomes in the surface waters of the North Pacific Subtropical Gyre (NPSG). We found diel cycles in pigment abundances resulting from the balance of their synthesis and consumption. The night represents a metabolic recovery phase to refill cellular pigment stores, while the photosystems are remodeled towards photoprotection during the day. Transcript levels of genes involved in photosynthesis and pigment metabolism had highly synchronized diel expression patterns among all taxa, suggesting that there are similar regulatory mechanisms for light and energy metabolism across domains, and that other environmental factors drive niche differentiation. Observed decoupling of diel oscillations in transcripts and related pigments in the NPSG indicates that pigment abundance is modulated by environmental factors extending beyond gene expression/regulation, showing that metatranscriptomes may provide only limited insights on real-time photophysiological metabolism.

Source connections

Explore related subjects

molecular biologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Becker, K. W., Harke, M. J., Mende, D. R., Muratore, D., Weitz, J. S., DeLong, E. F., Dyhrman, S. T., Van Mooy, B. A. S.. 2020-05-14. Combined pigment and metatranscriptomic analysis reveals synchronized diel patterns of phenotypic light response across domains in the open ocean. https://doi.org/10.1101/2020.05.12.091322

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Fatty Acid Synthase Binds Cellular mRNAs and its Depletion Reduces Translational Efficiency

Metabolic enzymes with non-canonical RNA binding activity have drawn a growing interest, due to their implications for basic biology and disease. Here we present the first endogenous RNA interactome of fatty acid synthase (FASN), an emerging oncological and virological target. Utilizing crosslinking-based approaches, we characterize the direct RNA association of FASN in two human cell lines, identifying over 6000 binding sites across over 3500 protein-coding genes, with a striking preference for the 5' UTR. We provide a functional cross-screen on the effects of FASN depletion on cellular translation. This integration with ribosome profiling indicated a preferential reduction in the translational efficiencies of FASN-associated mRNAs - an effect shown to be dependent on binding location and site number. Associated transcripts were enriched for morphogenic and cell division-related functions, as well as palmitoylated proteins. This correlative work primes further investigation of FASN as a regulator of translation of its target mRNAs.

molecular biology↗
bioRxiv2026

Genomic features and instability of linezolid resistance in vancomycin-resistant Enterococcus faecalis ST525

This study investigated the mechanisms of oxazolidinone resistance and genomic background in clinical ST525 Enterococcus faecalis isolates, a poorly characterized lineage reported in Brazilian hospitals as either vancomycin-resistant (VRE) or linezolid- and vancomycin-resistant (LVRE). Five LVREfs from intensive care unit patients (linezolid MICs, 8-32 mg/L; vancomycin MICs, >256 mg/L) carried only G2576T and G2505A (in three of four rrl copies) as known linezolid resistance determinants, despite variable linezolid MICs. During serial in vitro passages without antibiotic pressure, isolates with initial MICs of 8-16 mg/L exhibited progressive MIC reductions accompanied by reversion of mutant to wild-type rrl copies, whereas the isolate with an initial MIC of 32 mg/L maintained high-level resistance without reversion. Additional domain V substitutions emerged during MIC decline, while growth kinetics remained broadly similar. Whole-genome sequencing of a representative isolate (LVREfs L7) revealed a ~2.8-Mb chromosome enriched in mobile genetic elements (~8.6%), lacking a functional CRISPR-Cas system. A plasmid-borne prototype Tn1546 carrying vanA, devoid of internal insertion sequences, was found inserted into a Tn3-family transposase gene, a platform not typically associated with vanA mobilization. Together, these findings indicate that ST525 LVREfs, whose genomic features are consistent with long-term persistence in hospitals, may pose a challenge to routine susceptibility testing. A single mutational mechanism can yield variable linezolid MICs, and the ratio of mutated vs wild-type rrl copies can become heterogeneous in the absence of antibiotic pressure, without correlating directly with these values, contrary to the well-documented copy number-MIC correlation.

molecular biology↗
bioRxiv2026

Global repression of mesenchymal genes in epithelial cells by the histone demethylase LSD1

Epithelial-mesenchymal transition (EMT) is an essential process in development, tissue repair, and tumour metastasis, and is triggered by SNAI, ZEB and TWIST transcription factors, that recruit lysine-specific demethylase 1 (LSD1) to repress epithelial genes such as E-cadherin. In mesenchymal cells, LSD1 inhibition restores E-cadherin expression and reduces migration and invasion, consistent with LSD1 inhibition reverting EMT, and offering a therapeutic modality for EMT-associated disease. Recent data, however, suggest context-dependent roles for LSD1, as its inhibition in epithelial cells increases mesenchymal marker expression, potentially promoting EMT. To investigate this discrepancy, we mapped genome-wide binding of LSD1 in HCT116 epithelial cells and used rapid degron-mediated ablation of endogenous LSD1 to measure changes in nascent and steady-state transcription and chromatin accessibility. In epithelial cells, LSD1 binds constitutively-accessible, primed mesenchymal promoters. These are rapidly derepressed after LSD1 ablation, with activation of SNAI2 and ZEB1, which repress epithelial hallmarks such as E-cadherin. Re-introduction of LSD1 downregulates SNAI2 and ZEB1 but, surprisingly, further represses E-cadherin, indicating sustained loss of epithelial characteristics. Collectively, our results show that LSD1 maintains epithelial identity by repressing mesenchymal genes, questioning the therapeutic utility of LSD1 inhibition for EMT control.

molecular biology↗