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Results for “Biologic pathways”

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PubMed2002

Differential display analysis of gene expression in mammals: a p53 story.

Differential display is used worldwide as a method to identify changes in gene expression and to discover novel genes that are involved in important biological pathways. The principle of differential display is the systematic amplification of the 3' termini of messenger RNAs by using anchored oligo-dT primers in combination with upstream arbitrary primers. The separation of the polymerase chain reaction products by gel electrophoresis and their direct comparison allows the identification of differentially regulated genes. Recently, fluorescent differential display was established as the first nonradioactive differential display system with equivalent sensitivity to originally 33P isotopic labeling method. Because of its simplicity, sensitivity, reproducibility and automation, which increase the throughput and accuracy, differential display has become one of the most widely used gene-screening methods in biomedical research involving mammals. This chapter provides a glimpse of the application of differential display in search of target genes of the p53 tumor suppressor gene.

Animals↗

PubMed1999

The budding yeast cohesin gene SCC1/MCD1/RHC21 genetically interacts with PKA, CDK and APC.

Cohesin is a protein that plays a key role in the cohesion and separation of sister chromatids. During the duplication of chromatids, cohesin holds sister chromatids together until the onset of anaphase, and thereby prevents the premature separation of sister chromatids which would otherwise jeopardize the faithful segregation of chromosomes. To investigate the molecular mechanisms of sister chromatid cohesion, we have isolated multicopy suppressors of a temperature-sensitive (ts) mutation in the SCC1/MCD1/RHC21 gene which encodes a component of the cohesin complex in budding yeast. Isolation of multicopy suppressors of rhc21-sk16 and further genetic analyses revealed that several distinct biological pathways are involved in the regulation of SCC1/MCD1/RHC21 function. Firstly, PDE2 and BCY1, each of which inhibits the activity of protein kinase A (PKA), suppressed the temperature sensitivity of the rhc21-sk16 mutant. Secondly, PDE2 suppressed the temperature sensitivity of the cdc16-1 mutant. These results suggest that SCC1/MCD1/RHC21 is negatively regulated by the PKA pathway via the anaphase promoting complex (APC). Thirdly, ZDS1, a multicopy suppressor of cdc28-1N, and its homologue ZDS2 were isolated as multicopy suppressors of rhc21-sk16. Furthermore, the rhc21-sk16 mutant did not grow in the presence of the cdc28-1N mutation. Hence, SCC1/MCD1/RHC21 is positively regulated by the mitotic CDK, CDC28. Finally, SCC1/MCD1/RHC21 was found to interact genetically with CDC20, an activator of APC. Overexpression of CDC20 suppressed the temperature sensitivity of rhc21-sk16, and rhc21-sk16 was shown to be synthetically lethal with cdc20-1. In addition, the growth of the rhc21-sk16 mutant was inhibited by overproduction of the anaphase inhibitor Pds1p, whose degradation is mediated by Cdc20p in APC-dependent proteolysis. The functional relationships between SCC1/MCD1/RHC21 and PKA, CDK or APC are discussed.

Cdc20 Proteins↗

PubMed2025

High-fat and low-fat fermented milk and cheese intake, proteomic signatures, and risk of all-cause and cause-specific mortality.

PURPOSE: This study aimed to examine the associations between the intake of high- and low-fat fermented dairy (cheese and fermented milk), their proteomic profiles, and mortality risk. METHODS: This cohort study included 25,187 participants (mean age 57.7 years, 60.9% females). Fermented dairy intake was assessed by a modified diet history method. In a random subset of this cohort (n = 4359), we constructed proteomic signatures for fermented dairy intake using 136 candidate plasma proteins. RESULTS: During 23.5 years of follow-up, 9742 participants died. High-fat cheese (> 20% fat) intake was inversely associated with risk of all-cause mortality (HR for an increment of 20 g/day, 0.97; 95% CI, 0.96-0.99, P < 0.001) and cardiovascular disease mortality (HR, 0.96; 95% CI, 0.93-0.99, P = 0.006). Low-fat cheese intake showed an inverse association with all-cause mortality (HR, 0.98; 95% CI, 0.96-1.00, P = 0.047). Low-fat fermented milk intake was inversely associated with all-cause mortality (HR for an increment of 250 g/day, 0.91; 95% CI, 0.85-0.97, P = 0.006), while high-fat fermented milk (> 2.5% fat) showed null association. A total of 42, 26, 0, and 39 proteins were identified for the signature of high-fat cheese, low-fat cheese, high-fat fermented milk, and low-fat fermented milk, respectively. Inverse associations with all-cause mortality were observed for all three signatures with identified proteins. The identified proteins were involved in biological pathways related to immune response and inflammation. CONCLUSION: Our study indicated that consuming high-fat cheese, low-fat cheese, and low-fat fermented milk was linked to survival benefits. Plasma proteins improve our understanding of the health effects of fermented dairy.

Humans↗

PubMed2001

The maize WD-repeat gene ZmRbAp1 encodes a member of the MSI/RbAp sub-family and is differentially expressed during endosperm development.

Members of the MSI/RbAp sub-family of WD-repeat proteins are widespread in eukaryotic organisms and form part of multiprotein complexes that are involved in various biological pathways, including chromatin assembly, regulation of gene transcription, and cell division. In this study we report the isolation and characterization of a cDNA sequence from Zea mays, which encodes an RbAp-like protein (ZmRbAp1) that binds acetylated histones H3 and H4 and suppresses mutations that have a negative effect on the Ras/cAMP pathway in yeast. The ZmRbAp genes form a gene family and are expressed in different tissues of Z. mays L. plants. Determination of its expression pattern during maize seed development revealed that ZmRbAp transcripts are abundant during the initial stages of endosperm formation. In addition, the transcripts are specifically localized in shoot apical meristem and leaf primordia of the embryo. A possible role for the ZmRbAp genes in early endosperm differentiation and plant development is discussed.

Acetylation↗

PubMed2026

CRISPR-Enabled functional genomics in hPSCs-derived neural models for autism spectrum disorder.

Autism Spectrum Disorder (ASD) is a genetically heterogeneous neurodevelopmental condition in which hundreds of individually rare risk variants converge on a small number of shared biological pathways, including synaptic scaffolding, chromatin remodeling, excitation-inhibition balance, and cellular energy metabolism. Translating this genetic heterogeneity into mechanistic insight requires experimental systems capable of interrogating individual gene functions in human-relevant neural contexts at scale. CRISPR-enabled functional genomics in human pluripotent stem cell (hPSC)-derived neural models, spanning neural progenitors, cortical and inhibitory neurons, astrocytes, microglia, and brain organoids, provides precisely this capability. By integrating pooled perturbation screens with multimodal readouts including single-cell and spatial transcriptomics, chromatin accessibility profiling, proximity labeling proteomics, multi-electrode array electrophysiology, and metabolic flux analysis, these platforms enable systematic, causal mapping of ASD gene function at system resolution. Early applications have already revealed convergent mechanisms: BAF complex disruption expands the ventral progenitor pool and biases its fate toward oligodendrocyte and interneuron lineages; ADNP loss impairs microglial synaptic pruning through altered endocytic trafficking; and mTOR pathway dysregulation in PTEN- and TSC2-perturbed models links genetic risk directly to metabolic and mitochondrial dysfunction. Computational frameworks including MIMOSCA and SCEPTRE enable causal network reconstruction and pseudotime inference from these datasets, moving the field from gene lists toward pathway-level models of ASD pathobiology. Translational applications leverage isogenic iPSC panels and variant-level base and prime editing to stratify ASD variants by functional impact, informing gene therapy design for haploinsufficient targets such as CHD8 and SCN2A via AAV or antisense oligonucleotide delivery. Remaining challenges, including model developmental immaturity, batch variability, and the difficulty of modeling polygenic risk, are addressed by a roadmap integrating spatial perturbomics, AI-driven causal inference, and population-scale standardized biobanks. This review synthesizes the current state of CRISPR-based functional genomics in human stem cell neural models as a coherent experimental framework for converting ASD genetic associations into mechanistic understanding and therapeutic opportunity.

Humans↗

PubMed2024

Cohort Studies and Multi-omics Approaches to Low-Dose Ionizing Radiation-Induced Cardiovascular Disease: A Comprehensive Review.

The effect of low-dose ionizing radiation exposure on the risk of cardiovascular disease (CVD) represents a significant concern in the field of radiation protection. The prevailing approach to mitigating the adverse effects of low-dose or low-dose-rate radiation does not currently incorporate the potential risk of CVD, despite the possibility that such risk may be a substantial contributor to overall health hazards. Current evidence suggests a potential association between radiation exposure and CVD; however, the overall findings remain inconclusive. This is particularly due to the uncertainty surrounding the influence of significant non-radiation risk factors on the associations reported in epidemiological studies. It is difficult to discern the underlying connection in observational epidemiology when there is substantial variation in baseline risk factors. The paucity of epidemiological research in this domain is being partially offset by the advancement of multi-omics approaches. These methods assist in identifying radiosensitive targets, comprehending underlying biological processes, and pinpointing biomarkers. This, in turn, fortifies the evidence gleaned from epidemiological studies. In this review, we delve into the body of epidemiological research pertaining to CVD induced by low-dose ionizing radiation and the application of multi-omics techniques. The integration of these two methodologies holds the promise of identifying specific molecules or biological pathways that can be employed to validate endpoints related to radiation risk assessment.

Humans↗

PubMed1984

Abnormal abdominal computerized tomography with amiodarone therapy and clinical significance.

Although the antiarrhythmic agent, amiodarone, is known to cause elevation of liver function tests, the effect of this drug on abdominal computerized tomography (CT) scans in patients on amiodarone therapy is unknown. Since iodine is in its molecular structure, the presence of amiodarone or its metabolites might be expected to produce higher CT numbers similar to the effect of contrast agents. To test this hypothesis, CT scans were performed in a series of 25 patients receiving amiodarone, 14 receiving short-term (mean 2.5 +/- 1.3 days) and 19 receiving long-term therapy (mean 130 +/- 75 days), as well as in a control group not receiving amiodarone. Gastrointestinal symptoms (if any) and liver function tests (LFT) prior to instituting amiodarone therapy and at the time of CT scan were also documented. CT scans showed a modestly increased density in multiple organs in the short-term group, but a markedly increased hepatic density in all but one patient in the long-term group. Presence of gastrointestinal symptoms or abnormal LFT did not appear to correlate with the CT number. Such findings would suggest that increased hepatic density on CT scan is to be expected in patients receiving long-term amiodarone therapy, and although the exact biologic pathways of amiodarone metabolism are uncertain, the liver appears to be a major site of drug storage and/or metabolism.

Adult↗

PubMed1994

Sulfotransferase gene expression in rat hepatic and extrahepatic tissues.

Enzymatic sulfation has been implicated to play a key role in a number of essential biological pathways including xenobiotic detoxication, carcinogen activation, and the regulation of intra-tissue hormone activity. In order to increase our understanding of the critical determinants governing the regulation of sulfotransferase gene expression, we investigated age-, gender-, and xenobiotic-related alterations in hydroxysteroid sulfotransferase-a or aryl sulfotransferase-IV gene expression. Northern blot and slot blot analyses showed that rat hepatic hydroxysteroid sulfotransferase-a mRNA expression was responsive to age- and gender-related signals. The results also suggested that the rat hepatic aryl sulfotransferase-IV and hydroxysteroid sulfotransferase-a genes are differentially regulated. Northern blot and reverse transcriptase polymerase chain reaction analyses demonstrated that hydroxysteroid sulfotransferase-a mRNA was expressed to a greater extent in female rat liver than in lung or kidney tissue. In addition, rat hepatic hydroxysteroid sulfotransferase-a gene expression in mature female rats, although not substantially altered in response to short-term fasting or high-dose dexamethasone treatment, was suppressed after treatment with the polycyclic aromatic hydrocarbon, 3-methylcholanthrene.

Aging↗

PubMed1993

Nitric oxide synthase activity from a hematophagous insect salivary gland.

The salivary glands of the hematophagous insect, Rhodnius prolixus, contain a nitrosylhemeprotein that dissociates its ligand, NO, to the host tissues while the insect is searching for a blood meal. We now report a salivary nitric oxide synthase activity in this insect. The activity is dependent on NADPH, FAD, tetrahydrobiopterin, calmodulin, Ca2+, and converts arginine to citrulline while producing vasorelaxing activity. Molecular sieving indicates a molecular weight of 185 kDa, coeluting with a diaphorase activity. Results indicate similarity of this insect activity to the vertebrate constitutive NO synthase, suggesting NO synthesis is an evolutionary old biological pathway.

Amino Acid Oxidoreductases↗

PubMed1992

Bone hypertrophy and trabecular generation in Paget's disease and in fluoride-treated osteoporosis.

The replacement of lost trabeculae characteristic of postmenopausal osteoporosis is problematic, since a biological pathway has not been established for trabecular regeneration de novo in the healthy, intact, mature skeleton. Possible pathways for trabecular replacement may occur under pathological conditions, in particular those associated with bone hypertrophy. The topography of trabecular hypertrophy was compared in two groups of subjects with disease- or treatment-induced osteosclerosis following a period of atrophy. In Paget's disease and fluoride-treated osteoporosis a thickening of rarefied trabeculae in both was associated in Paget's disease only with an increase in the trabecular number and the transformation of a discontinuous arrangement into a more continuous network. The sequence seems to be a progression of intratrabecular resorption normally attendant upon a period of trabecular thickening. The failure of fluoride-treated bone in this respect, due to the unusual stability of the fluorotic skeleton, may provide insight to more effective anabolic regimens.

Adult↗

PubMed1986

Endometrial cancer and its precursors: a comparison of histological and clinical features.

In this study, the histological definition of endometrial cancer precursor (ECP) lesions is discussed and a comparison is made of clinical and histological parameters of ECP patients and endometrial cancer (EC) patients. ECP lesions were divided in 3 types: adenomatous hyperplasia, atypical hyperplasia and in situ adenocarcinoma. The following parameters were analyzed: age, menopausal status, gynecological and extragynecological familiar cancer incidence, other cancers in the proband, diabetes, obesity, primary infertility, fertility and previous estrogen therapy. Results give support to the hypothesis of the existence of a common biological pathway between ECP and EC. The high frequency of coexistence of both types of lesions in hysterectomy specimens from EC patients studied by step sections adds a confirmatory supporting argument. Measures for primary and secondary prevention of these lesions are proposed.

Adenocarcinoma↗

PubMed2025

Genetic analysis in African ancestry populations reveals genetic contributors to lung cancer susceptibility.

Striking disparities in lung cancer exist, with Black/African American individuals disproportionately affected by lung cancer, yet the genetic architecture in African ancestry individuals is poorly understood. We aimed to address this by performing a comprehensive genetic association study of lung cancer, incorporating local ancestry, across 6,490 African ancestry individuals (2,390 individuals with lung cancer and 4,100 control subjects). We identified a single genome-wide significant (p < 5 × 10-8) locus, 15q25.1 (lead SNP rs17486278, OR [95% CI] = 1.34 [1.23-1.45], p = 4.52 × 10-12), that has consistently shown a strong association with lung cancer across populations. Additionally, we identified nine suggestive (p < 1 × 10-6) loci. Four of these loci (3p12.1, 8q22.2, 14q11.2, and 18q22.3) have no prior reported associations with lung cancer. We performed a multi-ancestry lung cancer meta-analysis using prior large-scale summary statistics from European and Asian ancestry populations, incorporating our African ancestry results. The meta-analysis identified 17 genome-wide significant loci, including an association with locus 4q35.2 (p = 1.22 × 10-8), a genomic region that has been previously linked to forced expiratory volume. Genome-wide SNP-based heritability for lung cancer was 16% among African ancestry individuals. Follow-up in silico functional analyses identified genetically regulated gene expression (GReX) of nine genes (AC012184.3, ADK, CCDC12, CHRNA3, EML4, PSMA4, SNRNP200, TMEM50A, and ZYG11A) associated with lung cancer risk and biological pathways relevant to cancer and lung function. Cumulatively, these findings further elucidate the genetic architecture of lung cancer in African ancestry individuals, confirming prior loci and revealing new loci.

Female↗

PubMed2026

Handgrip strength and risk of common infections and sepsis: Two prospective cohorts with proteomic mediation analysis.

BACKGROUND: Recent evidence links adiposity with the risk of severe infections, but whether muscle strength may also be an independent risk factor is less studied. We investigated the association between handgrip strength and risk of common infections and sepsis and explored potential mediation by plasma proteomic biomarkers. METHODS: We analyzed data from 405,451 UK Biobank participants and replicated the main findings in 4474 Chinese adults from the Hong Kong Osteoporosis Study (HKOS). Baseline handgrip strength was measured by a dynamometer. Cox models were used to estimate its association with incidence of pneumonia, urinary tract infection (UTI), skin infection, and sepsis, adjusting for sociodemographic, lifestyle, and health-related factors. Mediation analyses were performed using 2912 plasma proteins in a UK Biobank subsample (n = 42,414) to identify biological pathways. RESULTS: In UK Biobank (median follow-up 13.6-15.3 years), lower handgrip strength was associated with significantly increased risk of pneumonia (hazard ratio per 5-kg decrement=1.10; 95% CI=1.09-1.11), UTI (1.10; 1.09-1.11), skin infection (1.05; 1.04-1.05), and sepsis (1.08; 1.07-1.10). Associations were largely consistent in HKOS, and the relative risks associated with low grip strength were generally most pronounced in underweight individuals. GDF15 and PLAUR were identified as the most important proteins which mediated 12-14% of these associations. CONCLUSION: Low handgrip strength is associated with increased risks of common infections and sepsis, particularly in underweight individuals, with partial mediation by proteins related to inflammation and immune-related pathways. Handgrip strength assessment may provide prognostic value beyond body mass index for clinical risk stratification.

Humans↗

PubMed2026

Unraveling causal links between chronic rhinosinusitis and peripheral artery diseases: insights from genetic correlations through genome-wide association studies.

OBJECTIVES: Chronic Rhinosinusitis (CRS) shares epidemiological links with Cardiovascular Diseases (CVDs), however, their shared genetic basis remains unclear. We hypothesized that pleiotropic genetic variants underlie CRS-CVDs links via distinct biological pathways. METHODS: Using large-scale GWAS data from European-ancestry individuals, we assessed global and local genetic correlations. We applied Genomic Structural Equation Modeling (Genomic SEM) to dissect shared genetic architecture, performed bidirectional Mendelian Randomization (MR) to infer causality, and conducted cis-eQTL colocalization to identify shared genetic signals. Finally, in vitro endothelial models (HUVECs) validated the functional dynamics of candidate genes under CRS-mimicking inflammatory stress. RESULTS: CRS showed significant genetic correlations with multiple CVDs. Genomic SEM revealed a latent factor structuring shared genetic risk through three pathways: artery diseases, myocardial diseases, and heart failure. Local genetic correlations identified significant local genetic correlations specifically between CRS and Peripheral Atherosclerosis (PAS)/Peripheral Artery Disease (PAD) specifically within the chr6: 31.57‒33.24 Mb locus. MR demonstrated causal effects of CRS on PAD (OR = 1.23, p = 0.022) and PAS (OR = 1.21, p = 0.011), but not vice versa. Genetically predicted HLA-DRB1, APOM, and COL11A2 expression conferred protection, while HLA-DQA2 increased risk. Crucially, in vitro validation corroborated these pathogenic trajectories, inflammatory stress significantly downregulated the protective APOM and upregulated the risk-associated HLA-DQA2 alongside pro-atherogenic VCAM-1, while HLA-DRB1 exhibited a compensatory upregulation (p < 0.05). CONCLUSION: CRS shares global genetic liability with CVDs, structured through three primary etiological pathways. Causal effects of CRS on peripheral artery diseases are mediated by immune and lipid-related genes within the chr6 locus, revealing divergent pleiotropic mechanisms. Our integrated genetic and in vitro evidence provides a mechanistic framework wherein chronic mucosal inflammation contributes to systemic endothelial vulnerability, thereby highlighting candidate targets for mechanism-directed therapy.

Humans↗

PubMed2026

Comprehensive mass spectrometry screening-derived atlas of HDAC inhibitors reveals histone-specific acetylation changes.

Histone deacetylase inhibitors (HDACis) have emerged as valuable therapeutics for cancer and other diseases; however, their effects on histone post-translational modification remain poorly characterized. Here, we applied quantitative mass spectrometry and high-throughput sequencing to systematically profile site-specific changes in histone modifications in response to a panel of HDACis. This platform enabled mapping of histone modification changes across hundreds of sites, including low-abundance histone marks. Furthermore, an integrative analysis of chromatin immunoprecipitation followed by sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) data identified genome-wide binding sites for the low-abundance histone modification of H2A.Z acetylation in HeLa and MDA-MB-231 breast cancer cells, highlighting the role of H2A.Z acetylation in regulating gene expression across diverse biological pathways, including specific genes involved in tumor suppressor pathways. Our findings provide a functional resource for identifying and quantifying histone modification changes and transcriptional regulation of histone H2A.Z acetylation following pharmacological perturbation.

Histone Deacetylase Inhibitors↗

PubMed2024

Gene expression patterns associated with PFOA exposure in Czech young men and women.

Perfluorooctanoic acid (PFOA), a member of per- and polyfluoroalkyl substances (PFASs), has been widely used in manufacturing for decades. Currently, PFOA is strictly regulated, but due to its high stability and persistence, it is detected in both environmental as well as in human matrices. To elucidate mechanisms of PFOA toxicity in humans, we determined the genome-wide transcriptomic changes of peripheral blood mononuclear cells (PBMC) responding to PFOA exposure in a sex-stratified analysis. This work employed samples from 145 female and 143 male participants of the CELSPAC: YA study to characterize PFOA-associated transcripts in a broader context using computational analysis. PFOA-associated gene expression differed significantly between men and women, as only 2 % of mapped genes were expressed in both sexes. Disease-specific enrichment analysis revealed cancer and immune-related disease terms as those most enriched in male and female populations. Patterns of enriched terms within the gene set enrichment analysis indicated three main targets of PFOA toxicity: i) lipid metabolism for women; ii) cell cycle regulation for men; and iii) immune system response for both sexes. In summary, our genome-wide transcriptomics analysis described sex-specific differences in PFOA-associated gene expression and provided evidence about biological pathways underlying PFOA toxicity in humans.

Humans↗

PubMed2026

Long-term (>7-year) parental consumption of genetically modified maize (Cry1Ab/Cry2Aj and EPSPS) induces no adverse sperm DNA methylation alterations across two generations of cynomolgus monkeys.

This study assessed the long-term safety of genetically modified (GM) maize from a male reproductive perspective, using a non-human primate model. We analyzed the sperm DNA methylation profiles in cynomolgus monkeys fed GM maize, non-GM parental maize, or a conventional diet over two generations (F0/F1). Whole-genome bisulfite sequencing (WGBS) revealed no significant differences in global methylation levels among groups. The identified differentially methylated regions (DMRs) were short, enriched in non-regulatory genomic areas, and did not cluster after treatment. Functional enrichment analysis showed that DMR-associated genes were consistently involved in the same core biological pathways (e.g., mTOR and Wnt signaling) across all dietary comparisons. These findings indicate that GM maize consumption did not induce specific adverse epigenetic alterations in sperm, with the observed changes reflecting common physiological adaptations to dietary variations rather than GM-related effects.

Animals↗

PubMed2026

Proteome Unravels Mechanism Differences in Embryogenesis Between Honey Bee Drone and Worker (Apis mellifera L.).

The physiological and social behaviors differ widely between honeybee workers and drones. All the organ rudiments of adult bees are formed during the embryonic stage. The initial molecular bases at the proteomic level for both embryonic developments have been identified, but a comprehensive understanding of the significant events involved in embryonic establishment remains elusive. To elucidate the molecular regulatory mechanisms underlying tissue differentiation during the embryogenesis of drones and workers, we implemented a state-of-the-art approach that combines in-hive inspection and targeted sampling (at nine embryogenesis stages) with high-throughput proteomics technology to investigate the developmental differences. In-hive inspection of hatching timing revealed an average developmental gap of approximately 3.6 h between the two embryos. Furthermore, proteomic analyses indicate that drone and worker embryos adopt distinct developmental strategies. Notably, proteins involved in fatty acid metabolism and key biological pathways related to organ formation-such as the Hedgehog and Wnt signaling pathways-are activated earlier in drones, suggesting that tissue development begins sooner in drone embryos than in workers. Additionally, the upregulation of cytoskeletal proteins and antioxidants in drone embryos likely supports their larger cell size and higher metabolic stress, reflecting distinct molecular characteristics of male development. Ribosomal proteins essential for biosynthetic support remain consistently expressed throughout the late stages in male embryos, indicating that drone embryogenesis lasts longer than that of workers. This work provides novel insights into the molecular foundations of honeybee embryogenesis and lays both theoretical and practical groundwork for future research into the mechanisms driving embryonic development.

Animals↗