bioRxiv Science⌕ Search

Biology subjects

Price, D.

Publications and source records attributed to Price, D..

At least 19 recordsLinked to original sources

Model Validation Protocols for Machine Learning in Small Molecule Drug Discovery

Machine learning (ML) models for molecular property prediction are increasingly deployed in drug discovery, yet their adoption in real-world scenarios requires an understanding of the conditions in which a model succeeds or fails. While standardized benchmarks are powerful instruments to measure and unlock progress in ML research, they should not be blindly treated as the end goal. Especially static and retrospective benchmarks, in which no true unknown test set is employed, limit our ability to robustly validate a model's performance. Building on the collective expertise of a cross-industry consortium, we present a model validation framework consisting of five recommendations that would enable the community to move beyond aggregate metrics toward understanding where and why molecular property prediction models fail. We connect evaluation choices to real-world applications and case studies encountered in pharmaceutical research. The framework proposes splitting strategies that mimic realistic distribution shifts and expose common failure modes. We apply the recommended framework to a recently released dataset of absorption, distribution, metabolism, and excretion (ADME) properties. Across two complementary model algorithms, our case studies reveal four distinct failure modes (extrapolation, interpolation, representation, and evaluation), showing that model errors arise not only from distribution shift but also from limitations in molecular representations. Our results show that commonly used evaluation protocols can significantly overestimate performance and may not detect important model failure modes. All software and data are released via https://github.com/srijitseal/polaris.

bioinformatics↗

DGAT1 as a Racially Divergent Driver of Carcinoma-Associated Fibroblast Activation Drives Tumorigenic Pathways via ERK1/2 Signaling in Prostate Cancer.

BackgroundThe incidence of lethal prostate cancer (PCa) is disproportionately higher in African American (AA) men compared to Caucasian (Cau) men. Racial differences in lipid reprogramming have been implicated in PCa progression. Recent studies identified race-specific biological alterations in carcinoma-associated fibroblasts (CAF). Here, we demonstrate that lipid-laden CAF from AA patients (AACAF) exhibits enhanced pro-tumorigenic functions compared to CAF from Cau patients (CauCAF). MethodsDGAT1-regulated genes in fibroblasts were identified by transcriptomic profiling, and their biological consequences were evaluated in vivo. Patient-derived CAF from AA and Cau men were examined to determine their molecular response to DGAT1 inhibition during tumorigenesis. ResultsLipid droplet (LD) biogenesis analysis revealed DGAT1-dependent LD accumulation in AACAF. DGAT1 overexpression in fibroblasts enhanced fibroblast activation protein (FAP1) expression and promoted in vivo tumorigenicity of cancer cells. Transcriptome and secretome profiling identified novel DGAT1-regulated genes associated with metabolism, cell-cell signaling, motility, and angiogenesis, largely mediated through the ERK1/2 pathway. Importantly, DGAT1 inhibition in patient-derived CAF elicited racially divergent regulation of pro-tumorigenic mediators, including BDNF, VEGF, and TSP1. ConclusionsOur findings reveal elevated DGAT1 expression in AACAF as a targetable enzymatic driver that enhances fibroblast activation and supports adaptation to a lipid-rich tumor microenvironment, thereby promoting tumorigenesis.

cancer biology↗

Cell-type specific iron content regulation revealed by single-cell iron quantification

Iron is crucial for cellular metabolism and cell growth. Nevertheless, in humans, both iron deficiency and disorders of iron overload are widespread. How cellular iron content varies depending upon iron availability, and how this influences cell function is poorly characterised. We developed a method to quantify metals in hundreds of cells per minute via single-cell inductively-coupled plasma mass spectrometry (sc-ICP-MS), and used this to explore iron usage by immune cells. Activated murine T-cells exposed to a 625-fold titration of extracellular iron maintained close homeostatic control, with iron content varying by [~]20%. However, these variations strongly correlated with activation characteristics and proliferation. Running sc-ICP-MS downstream of flow cytometric sorting showed that murine T-cells and B-cells ex vivo exhibit similar mean and heterogeneity of cellular iron while splenic macrophages contain twice as much iron and more heterogeneous iron content. Finally, activated human B-cells contain [~]10-fold more iron per cell than murine B-cells. We suggest that mechanisms of iron homeostasis impart particular ranges or set-points of iron content to different cell types and activation states, and that small changes in iron content have large effects on cell behaviour. Our methodological advance and consequent findings suggest new approaches to studying the biology of metals.

cell biology↗

Rapid and precise quantification of lymphocyte iron content by single cell inductively coupled plasma mass spectrometry

Metals facilitate catalysis during cellular metabolism, but heterogeneity of metal content at single-cell level within and between cell populations is poorly characterized. This is important because deficiencies of biometals, for example iron, are enormously prevalent worldwide. Here we quantify metal content of single-cells using inductively-coupled plasma mass spectrometry. To develop the method, we used rhodium and iridium-intercalated Jurkat cells, obtaining >0.96% r2 cross-analytical correlation with mass cytometry. We quantified iron and calcium mass/cell for murine T-lymphocytes with 3% and 8% 2-sigma intra-precision, respectively, when assessing thousands of cells/minute. T-lymphocytes exposed to a 625-fold difference in extracellular iron concentrations maintained close iron homeostatic control, varying [~]20% in iron content. Nevertheless, this relatively small variation strongly correlated with changes in cellular activation characteristics measured by flow cytometry. We also assessed human B-cell iron content, which was [~]10-fold higher than murine T-lymphocytes. Overall, we demonstrate rapid iron quantification at single-cell level in different cell types and relate cellular iron content to cell function. TeaserPrecise and rapid iron metallomics of lymphocytes by single cell ICP-MS is a powerful approach for accessing signatures of immunological status.

immunology↗

Splicing-aware resolution of scRNA-Seq data

Single-cell RNA sequencing (scRNA-Seq) provides invaluable insights in cell biology. Current scRNA-Seq analytic approaches do not distinguish between spliced and unspliced mRNA. RNA velocity paradigm suggests that the presence of unspliced mRNA reflects transitional cell states, informative for studies of dynamic processes such as embryogenesis or tissue regeneration. Alternatively, stable cell subsets may also maintain unspliced mRNA reservoirs for prompt initiation of transcription-independent expression. Based on the latter paradigm, we have developed a method called SANSARA (Splicing-Aware scrNa-Seq AppRoAch) for the splicing-aware analysis of scRNA-Seq data. We employed SANSARA to characterize peripheral blood regulatory T cell (Treg) subsets, revealing the complex interplay between FoxP3 and Helios master transcription factors and other unexpected splicing-informed features. For Th1 and cytotoxic CD4+ T cell subsets, SANSARA also revealed substantial splicing heterogeneity across crucial subset-specific genes. SANSARA is straightforward to implement in current data analysis pipelines and opens new dimensions in scRNA-Seq-based discoveries.

immunology↗

The expression of PKM1 and PKM2 in developing, benign, and cancerous prostatic tissues

Neuroendocrine prostate cancer (NEPCa) is the most aggressive type of prostate cancer. However, energy metabolism, one of the hallmarks of cancer, in NEPCa has not been well studied. Pyruvate kinase M (PKM), which catalyzes the final step of glycolysis, has two main splicing isoforms, PKM1 and PKM2. PKM2 is known to be upregulated in various cancers, including prostate adenocarcinoma (AdPCa). In this study, we used immunohistochemistry, immunofluorescence staining, and bioinformatic analysis to examine the expression of PKM1 and PKM2 in mouse and human prostatic tissues, including developing, benign and cancerous prostate. We found that PKM2 was the predominant isoform expressed throughout prostate development and PCa progression, with slightly reduced expression in some NEPCa samples. PKM1 was mostly expressed in stromal cells but low-level PKM1 was also detected in prostate basal epithelial cells. Its expression was absent in the majority of PCa specimens but present in a subset of NEPCa. Additionally, we evaluated the mRNA levels of ten PKM isoforms that express exon 9 (PKM1-like) or exon 10 (PKM2-like). Some of these isoforms showed notable expression levels in PCa cell lines and human PCa specimens. These findings lay the groundwork for understanding PKMs role in PCa carcinogenesis and NEPCa progression. The distinct expression pattern of PKM isoforms in different PCa subtypes may offer insights into potential therapeutic strategies for treating PCa.

cancer biology↗

DHODH inhibition enhances the efficacy of immune checkpoint blockade by increasing cancer cell antigen presentation

Pyrimidine nucleotide biosynthesis is a druggable metabolic dependency of cancer cells, and chemotherapy agents targeting pyrimidine metabolism are the backbone of treatment for many cancers. Dihydroorotate dehydrogenase (DHODH) is an essential enzyme in the de novo pyrimidine biosynthesis pathway that can be targeted by clinically approved inhibitors. However, despite robust preclinical anticancer efficacy, DHODH inhibitors have shown limited single-agent activity in phase 1 and 2 clinical trials. Therefore, novel combination therapy strategies are necessary to realize the potential of these drugs. To search for therapeutic vulnerabilities induced by DHODH inhibition, we examined gene expression changes in cancer cells treated with the potent and selective DHODH inhibitor brequinar (BQ). This revealed that BQ treatment causes upregulation of antigen presentation pathway genes and cell surface MHC class I expression. Mechanistic studies showed that this effect is 1) strictly dependent on pyrimidine nucleotide depletion, 2) independent of canonical antigen presentation pathway transcriptional regulators, and 3) mediated by RNA polymerase II elongation control by positive transcription elongation factor B (P-TEFb). Furthermore, BQ showed impressive single-agent efficacy in the immunocompetent B16F10 melanoma model, and combination treatment with BQ and dual immune checkpoint blockade (anti-CTLA-4 plus anti-PD-1) significantly prolonged mouse survival compared to either therapy alone. Our results have important implications for the clinical development of DHODH inhibitors and provide a rationale for combination therapy with BQ and immune checkpoint blockade.

cancer biology↗

16p11.2 locus decelerates subpallial maturation and limits variability in human iPSC-derived ventral telencephalic organoids

Inhibitory interneurons regulate the activity of cortical circuitry, and their dysfunction has been implicated in Autism Spectrum Disorder (ASD). 16p11.2 microdeletions are genetically linked to 1% of ASD. However, there have been few studies of the effects of this microdeletion on interneuron development. Using ventral telencephalic organoids derived from human induced pluripotent stem cells, we investigated the effect of this microdeletion on organoid size, progenitor proliferation and organisation into neural rosettes, ganglionic eminence (GE) marker expression at early developmental timepoints and expression of the neuronal marker, NEUN at later stages. Early deletion organoids exhibited significantly greater variations in size with concomitant increases in relative neural rosette area and the expression of the ventral telencephalic marker, COUPTFII, with significantly increased variability in these properties. Cell cycle analysis revealed a significant increase in total cell cycle length caused primarily by an elongated G1-phase, the duration of which also varied significantly more than normal. Late deletion organoids increased their expression of the neuronal marker NEUN. We propose that 16p11.2 microdeletions increase developmental variability and may contribute to ASD aetiology by lengthening the cell cycle of ventral progenitors, promoting premature differentiation into interneurons. Summary StatementUsing 3D-region-specific organoids, we demonstrate that 16p11.2 deletion increases variability and prolongs the cell cycle of human subpallial progenitors by lengthening their G1 phase.

developmental biology↗

Epigenetic Memory of COVID-19 in Innate Immune Cells and Their Progenitors

Severe coronavirus disease 2019 (COVID-19) is characterized by systemic inflammation and can result in protracted symptoms. Robust systemic inflammation may trigger persistent changes in hematopoietic cells and innate immune memory through epigenetic mechanisms. We reveal that rare circulating hematopoietic stem and progenitor cells (HSPC), enriched from human blood, match the diversity of HSPC in bone marrow, enabling investigation of hematopoiesis and HSPC epigenomics. Following COVID-19, HSPC retain epigenomic alterations that are conveyed, through differentiation, to progeny innate immune cells. Epigenomic changes vary with disease severity, persist for months to a year, and are associated with increased myeloid cell differentiation and inflammatory or antiviral programs. Epigenetic reprogramming of HSPC may underly altered immune function following infection and be broadly relevant, especially for millions of COVID-19 survivors. One Sentence SummaryTranscriptomic and epigenomic analysis of blood reveal sustained changes in hematopoiesis and innate immunity after COVID-19. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=197 HEIGHT=200 SRC="FIGDIR/small/479588v1_ufig1.gif" ALT="Figure 1"> View larger version (54K): org.highwire.dtl.DTLVardef@1ffe42dorg.highwire.dtl.DTLVardef@dd4868org.highwire.dtl.DTLVardef@1bcae8borg.highwire.dtl.DTLVardef@674e85_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Auto-Immunoproteomics Analysis of COVID-19 ICU Patients Revealed Increased Levels of Autoantibodies Related to Male Reproductive System

The role of autoantibodies in coronavirus disease (COVID-19) complications is not yet fully understood. The current investigation screened two independent cohorts of 97 COVID-19 patients (Discovery (Disc) cohort from Qatar (n = 49) and Replication (Rep) cohort from New York (n = 48)) utilizing high-throughput KoRectly Expressed (KREX) immunome protein-array technology. Autoantibody responses to 57 proteins were significantly altered in the COVID-19 Disc cohort compared to healthy controls (P [≤] 0.05). The Rep cohort had altered autoantibody responses against 26 proteins compared to non-COVID-19 ICU patients that served as controls. Both cohorts showed substantial similarities (r2 = 0.73) and exhibited higher autoantibodies responses to numerous transcription factors, immunomodulatory proteins, and human disease markers. Analysis of the combined cohorts revealed elevated autoantibody responses against SPANXN4, STK25, ATF4, PRKD2, and CHMP3 proteins in COVID-19 patients. KREX analysis of the specific IgG autoantibody responses indicates that the targeted host proteins are supposedly increased in COVID-19 patients. The autoantigen-autoantibody response was cross-validated for SPANXN4 and STK25 proteins using Uniprot BLASTP and sequence alignment tools. SPANXN4 is essential for spermiogenesis and male fertility, which may predict a potential role for this protein in COVID-19 associated male reproductive tract complications and warrants further research. Significance StatementCoronavirus disease (COVID-19), caused by the SARS-CoV-2 virus, has emerged as a global pandemic with a high morbidity rate and multiorgan complications. It is observed that the host immune system contributes to the varied responses to COVID-19 pathogenesis. Autoantibodies, immune system proteins that mistakenly target the bodys own tissue, may underlie some of this variation. We screened total IgG autoantibody responses against 1,318 human proteins in two COVID-19 patient cohorts. We observed several novel markers in COVID-19 patients that are associated with male fertility, such as sperm protein SPANXN4, STK25, and the apoptotic factor ATF4. Particularly, elevated levels of autoantibodies against the testicular tissue-specific protein SPANXN4 offer significant evidence of anticipating the protein role in COVID-19 associated male reproductive complications.

immunology↗

Altered basal lipid metabolism underlies the functional impairment of naive CD8+ T cells in elderly humans

BackgroundAging is associated with functional deficits in the naive T cell compartment, which compromise the generation of de novo immune responses against previously unencountered antigens. The mechanisms that underlie this phenomenon have nonetheless remained unclear. MethodsBiochemical and functional properties of naive CD8+ T cells were characterized and compared between middle aged and older individuals. FindingsWe identified an age-related link between altered basal lipid metabolism in naive CD8+ T cells and their impaired responsiveness to stimulation, characterized by low proliferative potential and susceptibility to apoptosis. Reversal of the bioenergetic anomalies with lipid-altering drugs, such as rosiglitazone, improved the functional capabilities of naive CD8+ T cells in elderly subjects. InterpretationInterventions that favor lipid catabolism may find utility as adjunctive therapies in the elderly to promote vaccine-induced immunity against emerging pathogens or tumors. FundingA full list of the funding sources is detailed in the Acknowledgment section of the manuscript. RESEARCH IN CONTEXTO_ST_ABSEvidence before this studyC_ST_ABSOld subjects are highly susceptible to infections and tumors and usually present with low responses to vaccine. This is mainly due to the age-related loss of primary immune resources, i.e. a quantitative decline of naive CD8+ T cells. Nonetheless, few studies have also underlined, within this cell subset, qualitative defects in elderly subjects. Added value of this studyConsidering the well-demonstrated link between nutrient usage and lymphocyte functions, we characterized the bioenergetics features of old naive CD8+ T cells. Our data show an age-dependent altered basal metabolism in this cell subset, mostly at the levels of fatty acids and mitochondrial functions. These alterations were associated with functional defects which were partially reverted through the use of lipid-lowering strategies. Implications of all the available evidenceThis study highlights the potential role of an altered cellular lipid metabolism in immunosenescence, providing clues to understand the epidemiological profile of emerging infections or tumors and to develop preventive and therapeutic strategies based on metabolic manipulation.

immunology↗

The identity of human tissue-emigrant CD8+ T cells

Lymphocyte migration is essential for human adaptive immune surveillance. However, our current understanding of this process is rudimentary, because most human studies to date have been restricted to immunological analyses of blood and various tissues. To address this issue, we used an integrated approach to characterize tissue-emigrant immune cells in thoracic duct lymph (TDL). In humans and non-human primates, lymphocytes were by far the most abundant immune lineage population in efferent lymph, and a vast majority of these lymphocytes were T cells. Cytolytic CD8+ T cell subsets were clonotypically discrete and selectively confined to the intravascular circulation, persisting for months after inhibition of S1P-dependent tissue egress by FTY-720. In contrast, non-cytolytic CD8+ T cell subsets with stem-like epigenetic and transcriptional signatures predominated in tissues and TDL. Collectively, these data provide an atlas of the migratory immune system and define the nature of tissue-emigrant CD8+ T cells that recirculate via TDL.

immunology↗

Dystrophic microglia are a disease associated microglia morphology in the human brain

Microglia activation--typically described in terms of hypertrophic appearance--is a well-established feature of aging. Recent studies have suggested that microglia dystrophy, not activation, may increase the propagation of progressive neurodegenerative diseases such as Alzheimers disease (AD). Yet, a clear understanding of cause and consequences of dystrophic microglia is lacking. Although frequently observed in diseased brains, the appearance of dystrophic microglia in the hippocampus of individuals free of cognitive impairment suggests that microglia may be undergoing senescence with age, leading to dystrophy. Therefore, we hypothesized that chronological age could be a significant contributor to the presence of dystrophic microglia. To investigate this relationship, we employed stereological counts of total microglia, hypertrophic, and dystrophic microglia across the decades of the human lifespan. The microglia counts were performed in the frontal cortex gray and white matter and the CA1 subregion of the hippocampus in individuals without known neurodegenerative disease. There was age-associated increase in the number of dystrophic microglia in the CA1 region and the frontal cortex gray matter related to age. However, the increase in dystrophic microglia was proportional to the age-related increase in the total number of microglia, suggesting that aging alone was not sufficient to explain the presence of dystrophic microglia. We next tested if dystrophic microglia could be a disease-associated microglia phenotype. Compared to controls without neuropathology, the number of dystrophic microglia was significantly greater in aged-matched cases with either AD, dementia with Lewy bodies, or LATE-NC. These results provide evidence that healthy aging is only associated with a modest increase in dystrophic microglia and suggest that dystrophic microglia may be a disease-associated microglia phenotype. Finally, we found strong evidence for iron homeostasis changes, with increases in ferritin light chain, in dystrophic microglia compared to ramified or hypertrophic microglia. Based on our findings, microglia dystrophy, and not hypertrophic microglia, are the disease-associated microglia morphology. Future work is required to understand the links between the increase in dystrophic microglia and neurodegenerative disorders.

neuroscience↗

Transient resting-state network dynamics in cognitive ageing

It is important to maintain cognitive function in old age, yet the neural substrates that support successful cognitive ageing remain unclear. One factor that might be crucial, but has been overlooked due to limitations of previous data and methods, is the ability of brain networks to flexibly reorganise and coordinate over a millisecond time-scale. Magnetoencephalography (MEG) provides such temporal resolution, and can be combined with Hidden Markov Models (HMMs) to characterise transient neural states. We applied HMMs to resting-state MEG data from a large cohort (N=594) of population-based adults (aged 18-88), who also completed a range of cognitive tasks. Using multivariate analysis of neural and cognitive profiles, we found that decreased occurrence of "lower-order" brain networks, coupled with increased occurrence of "higher-order" networks, was associated with both increasing age and impaired fluid intelligence. These results favour theories of age-related reductions in neural efficiency over current theories of age-related functional compensation.

neuroscience↗

A whole-genome scan for association with invasion success in the fruit fly Drosophila suzukii using contrasts of allele frequencies corrected for population structure

Evidence is accumulating that evolutionary changes are not only common during biological invasions but may also contribute directly to invasion success. The genomic basis of such changes is still largely unexplored. Yet, understanding the genomic response to invasion may help to predict the conditions under which invasiveness can be enhanced or suppressed. Here we characterized the genome response of the spotted wing drosophila Drosophila suzukii during the worldwide invasion of this pest insect species, by conducting a genome-wide association study to identify genes involved in adaptive processes during invasion. Genomic data from 22 population samples were analyzed to detect genetic variants associated with the status (invasive versus native) of the sampled populations based on a newly developed statistic, we called C2, that contrasts allele frequencies corrected for population structure. This new statistical framework has been implemented in an upgraded version of the program BO_SCPLOWAYC_SCPLOWPO_SCPLOWASSC_SCPLOW. We identified a relatively small set of single nucleotide polymorphisms (SNPs) that show a highly significant association with the invasive status of populations. In particular, two genes RhoGEF64C and cpo, the latter contributing to natural variation in several life-history traits (including diapause) in Drosophila melanogaster, contained SNPs significantly associated with the invasive status in the two separate main invasion routes of D. suzukii. Our methodological approaches can be applied to any other invasive species, and more generally to any evolutionary model for species characterized by non-equilibrium demographic conditions for which binary covariables of interest can be defined at the population level.

evolutionary biology↗

On the evolution of neural decisions from uncertain visual input to uncertain actions

Behavior can be conceived as the result of a sequence in which the outcomes of perceptual decisions inform decisions on which action to take. However, the relationship between these processes, and spatiotemporal dynamics of the visual-to-motor transformation remains unclear. Here, we combined accumulation-to-threshold models and electro-magnetoencephalography, to trace neural correlates of sensorimotor decisions in space, time and frequency. We challenge the assumption of sequential decisions, with evidence that visuomotor processing unfolds through a continuous flow of information from sensory to motor regions. Action selection is initiated before regional visual decisions are completed. By linking behavior and physiology through theoretical decision models, we identify simultaneous forward and backward flow of information for visuomotor decisions between sensory and motor regions, in beta and gamma ranges. The model of integrated visuomotor decisions provides a powerful approach to investigate behavioral disorders that impair the ability to use sensory inputs to guide appropriate actions.

neuroscience↗

Self-reported sleep relates to hippocampal atrophy across the adult lifespan - results from the Lifebrain consortium

BackgroundPoor sleep is associated with multiple age-related neurodegenerative and neuropsychiatric conditions. The hippocampus plays a special role in sleep and sleep-dependent cognition, and accelerated hippocampal atrophy is typically seen with higher age. Hence, it is critical to establish how the relationship between sleep and hippocampal volume loss unfolds across the adult lifespan.\n\nMethodsSelf-reported sleep measures and MRI-derived hippocampal volumes were obtained from 3105 cognitively normal participants (18-90 years) from major European brain studies in the Lifebrain consortium. Hippocampal volume change was estimated from 5116 MRIs from 1299 participants, covering up to 11 years. Cross-sectional analyses were repeated in a sample of 21390 participants from the UK Biobank.\n\nResultsThe relationship between self-reported sleep and age differed across sleep items. Sleep duration, efficiency, problems, and use of medication worsened monotonously with age, whereas subjective sleep quality, sleep latency, and daytime tiredness improved. Women reported worse sleep in general than men, but the relationship to age was similar. No cross-sectional sleep - hippocampal volume relationships was found. However, worse sleep quality, efficiency, problems, and daytime tiredness were related to greater hippocampal volume loss over time, with high scorers showing on average 0.22% greater annual loss than low scorers. Simulations showed that longitudinal effects were too small to be detected as age-interactions in cross-sectional analyses.\n\nConclusionsWorse self-reported sleep is associated with higher rates of hippocampal decline across the adult lifespan. This suggests that sleep is relevant to understand individual differences in hippocampal atrophy, but limited effect sizes call for cautious interpretation.

neuroscience↗

Kingdom-wide comparison reveals conserved diurnal gene expression in Archaeplastida

Plants have adapted to the diurnal light-dark cycle by establishing elaborate transcriptional programs that coordinate innumerable metabolic, physiological, and developmental responses to the external environment. These transcriptional programs have been studied in only a few species, and their function and conservation across algae and plants is currently unknown. We performed a comparative transcriptome analysis of the diurnal cycle of nine members of Archaeplastida, and we observed that, despite large phylogenetic distances and dramatic differences in morphology and lifestyle, diurnal transcriptional programs of these organisms are similar. However, the establishment of multicellularity coincided with the uncoupling of cell division from the diurnal cycle and decreased diurnal control of the expression of the biological pathways. Hence, our study provides evidence for the universality of diurnal gene expression and elucidates its evolutionary history among different photosynthetic eukaryotes.

evolutionary biology↗