Biology subjects

Berger, S.

Publications and source records attributed to Berger, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Conserved role of EGFR signaling in apoptotic cell recognition and processing across different phagocytes

Efferocytosis is an essential process that clears dying cells from tissues and prevents inflammation. However, the mechanisms by which apoptotic cells recruit and activate phagocytes remain poorly understood. Here, we show that EGFR signaling is both necessary and sufficient for efficient efferocytosis in two diverse phagocytes: the gonadal sheath cells of C. elegans and the zebrafish microglia. In C. elegans, loss of LET-23 EGFR or its downstream effector MPK-1 ERK in the sheath cells impairs the recognition and degradation of apoptotic germ cells. Germ cells undergoing apoptosis secrete the EGF ligand LIN-3, which promotes their recognition and engulfment. Overexpression of EGF in non-apoptotic germ cells is sufficient to trigger their engulfment, indicating that EGF can function as an engulfment signal independently of apoptotic cell death. In zebrafish larvae, pharmacological inhibition of EGFR signaling reduces microglial motility, recognition of apoptotic neurons, and corpse clearance in the optic tectum. Similar to C. elegans, an ectopic source of EGF serves as an attractive cue that promotes microglial recruitment. Our findings suggest that EGFR signaling controls an evolutionarily conserved efferocytosis module that coordinates the recognition and processing of apoptotic corpses in different types of phagocytes.

cell biology↗

bioRxiv2026

Dendritic excitatory-inhibitory balance and branch-specific gating enable selective recall of associative memories

The ability to reconstruct complete memories from fragmented cues is a defining feature of associative memory, which requires neural circuits to store many overlapping and conflicting memory representations while selectively controlling memory accessibility. Attractor dynamics provide the dominant modelling framework for associative memory and have been used to interpret connectivity and behaviour. Yet despite this influence, how attractor-based memory is implemented in biophysical spiking circuits with compartmental dendrites and structured recurrent interactions has remained unresolved, with no unifying theoretical framework for interpreting emerging dendritic imaging and connectomic data. Here we show that local dendritic excitatory-inhibitory balance creates binary-like membrane-potential states that enable associative recall, and that branch-selective inhibition gates access to memory sets stored across dendritic trees, limiting interference between distinct sets. We further show that continuous dendritic dynamics enlarge basins of attraction by integrating partial cues over time, and that a winner-take-all readout circuit implements memory-set selection autonomously, generating interneuron activity that encodes set identity. Our framework predicts branch-specific voltage and calcium signatures that provide a basis for interpreting dendritic measurements in terms of engram organisation, bridging classical associative memory theory with dendritic circuit mechanisms.

neuroscience↗

bioRxiv2026

Transcriptional feedback targeting Wnt pathway components reveals hidden heterogeneity in C. elegans seam cell lineages.

Asymmetric cell division in the epidermal stem cells of Caenorhabditis elegans, known as seam cells, relies on the Wnt/{beta}-catenin asymmetry pathway to generate daughter cells with distinct fates. However, whether components of this pathway components are transcriptionally regulated during these divisions remains unclear. Here, we employ single molecule fluorescence in situ hybridisation to quantify mRNA distributions of key Wnt pathway components during L2 symmetric and asymmetric seam cell divisions. We find that transcripts encoding the negative regulators pry-1/Axin and apr-1/APC are enriched in posterior daughter cells, while those encoding the positive regulators sys-1/{beta}-catenin, wrm-1/{beta}-catenin, and lit-1/NLK, along with the transcription factor pop-1/TCF, are enriched in anterior daughter cells. Strikingly, molecular asymmetries are already evident following the L2 symmetric division, with anterior and posterior daughters exhibiting distinct levels of Wnt component expression and Wnt pathway activation. These mRNA distributions are surprising considering the established protein localisations that underpin the Wnt asymmetry model and suggest extensive post-divisional transcriptional regulation. We further demonstrate that pop-1 asymmetric expression depends on Wnt signalling activity, supporting a model in which transcriptional feedback reinforces cell fate decisions. Investigation of protein distributions using knock-in reporters for PRY-1 and CAM-1 showed that protein accumulation patterns at L2 are consistent with transcript levels. Our findings uncover pervasive transcriptional feedback within the Wnt pathway that likely contributes to robust fate specification and reveal molecular heterogeneity with potential functional consequences for lineage behaviour.

developmental biology↗

bioRxiv2026

Rescue of pATOM36-depleted T. brucei by human MTCH1/2 reveals common features of protein insertases

Alpha-helically anchored proteins of the mitochondrial outer membrane depend on dedicated insertases, including the MIM complex in yeast, pATOM36 in trypanosomes, and MTCH1/MTCH2 in humans. These insertases lack sequence homology and arose by convergent evolution. Here we show that MTCH1 and an N-terminally modified MTCH2 can replace the OMM biogenesis function of trypanosomal pATOM36, demonstrating functional compatibility across a large phylogenetic distance. Moreover, like other insertases, pATOM36 has lipid scramblase activity and likely induces local membrane thinning. Structural modeling reveals that even though they have inverted membrane topologies, pATOM36 and MTCH1/MTCH2 adopt a similar architecture. They form a hydrophilic cavity comprising five transmembrane helices that is open to both the cytosol and laterally to the membrane core. The same features also extend to the large phylogenetically unrelated YidC-like insertase family of bacterial origin. Together, these findings suggest that membrane protein insertion is constrained to a small number of viable mechanistic solutions, providing evidence for "deterministic" evolution acting at the molecular level.

biochemistry↗

bioRxiv2026

Ancient origin of the dorso-ventral patterning system of vertebrate paired fins

The origin of paired fins was a major event in early vertebrate history that fuelled the adaptive radiation of the gnathostome clade. Evidence for the conservation of ancient regulatory systems between paired and median fins supports a model in which appendage-patterning mechanisms first evolved in the midline and were later redeployed to a new embryonic context, the flank. However, while paired fins and limbs are asymmetric along the dorso-ventral (DV) axis, the equivalent axis does not exist in median fins, which are symmetric across the midline, raising questions of how DV patterning evolved. Here, we combine genetic tools in zebrafish with comparative expression analyses in representative ray-finned and cartilaginous fishes to show that a subset of limb dorsoventral (DV) patterning genes are expressed during median fin development. Using genetic lineage tracing of the canonical limb dorsalizing factor lmx1bb, we further demonstrate that, although lmx1bb-derived cells occupy distinct spatial domains across fin types, a subset of this lineage is fated to differentiate into fin-ray osteoblasts in both paired and median fins. To test the potential conservation of regulatory modules across fin types, we generated a series of deletion mutants for two known lmx1b mouse limb enhancers, LARM1 and LARM2, that we show are partially conserved upstream of zebrafish lmx1bb. These experiments revealed that LARM function is essential for dorsoventral patterning in the paired pectoral and pelvic fins of zebrafish but is dispensable for formation of the unpaired dorsal and anal fins. To determine if the paired fin specificity of LARM-mediated lmx1b regulation is a feature of more basal gnathostomes, we used a single cell multiomics (RNAseq + ATACseq) approach in the epaulette shark Hemiscyllium ocellatum, a representative chondrichthyan and outgroup to osteichthyans. Strikingly, these analyses demonstrated linkages between the LARM1 enhancer and lmx1b in the unpaired dorsal fins of epaulette sharks, as well as the deployment of a Lmx1b-mediated regulatory network whose core downstream components are conserved between dorsal fins, paired fins, and limbs. Collectively, these data support the ancient origin of a "DV" regulatory module in median fins that was redeployed during the early evolution paired fins, facilitating the assembly of the DV patterning axis. Intriguingly, multiome-based inference of global fin network architecture in epaulette shark also revealed reduced regulatory complexity in pectoral relative to median fins, suggesting that co-option as a mechanism for anatomical innovation can proceed through selective streamlining of ancestral network components.

developmental biology↗

bioRxiv2026

A Spinal Muscular Atrophy Model Reveals Both Developmental and Degenerative Neuronal Defects in C. elegans

Spinal muscular atrophy (SMA) is a neuromuscular disorder primarily caused by mutations in the Survival of Motor Neuron 1 (SMN1) gene. SMN1 is ubiquitously expressed and encodes a protein essential for the assembly of small nuclear ribonucleoproteins (snRNPs), key components of pre-mRNA splicing. Beyond this canonical role, SMN participates in several other fundamental cellular processes, including RNA transport, regulation of actin dynamics, transcription, and translation. While multiple hypotheses have been put forward to explain selective motor neuron (MN) vulnerability to SMN deficiency, the precise mechanisms involved remain incompletely understood. In this study, we used a simple and tractable C. elegans model to investigate the molecular mechanisms underlying neuronal degeneration in SMA. Silencing of the smn-1 in targeted neurons resulted in defects in the birth and development of both motor neurons and touch receptor neurons (TRNs). In TRNs SMN-1 depletion caused distinct defects in neuronal process morphology. Our results provide evidence that key aspects of SMA pathology are conserved in C. elegans, which may offer new opportunities to elucidate the molecular mechanisms underlying neuronal degeneration in SMA.

genetics↗

bioRxiv2025

Protein-protein interactions drive differences in the spatiotemporal dynamics of transcription factors NANOG and SOX2 in naïve pluripotent cells

Maintenance of naive pluripotency requires core transcription factors (TFs) like SOX2 and auxiliary TFs like NANOG, yet molecular mechanisms governing their intra-nuclear dynamics and DNA binding interactions remain unclear. Here, using high-density 3D single-molecule light-field microscopy combined with novel spatiotemporal analysis pipelines, we track SOX2 and NANOG dynamics in live cells. Despite lower protein abundance, NANOG displays a similar chromatin-bound fraction to SOX2. This arises partially because, while both TFs undergo frequent transient non-specific binding interactions ([~]0.5-0.7s), NANOG exhibits more stable specific binding ([~]25s vs [~]16s). Both TFs also assemble into phase-separated domains of [~]400 nm containing both freely diffusing and chromatin-bound proteins, which further influences their dynamics. Strikingly, NANOGs protein-protein interaction domain markedly increases chromatin residence time (>5-fold) and the size of these phase-separated domains. Our work uncovers how NANOG and SOX2 stabilise gene regulatory networks that maintain naive pluripotency while providing quantitative pipelines for dissecting spatiotemporal TF dynamics.

cell biology↗

bioRxiv2024

The clumped isotope signatures of multiple methanogenesis metabolisms

Methane is a potent greenhouse gas, an important energy source, and a potential biosignature on extraterrestrial planetary bodies. The relative abundances of doubly substituted ("clumped") methane isotopologues (13CH3D and 12CH2D2) offer important information on the sources and sinks of methane. However, the clumped isotope signatures of microbially produced methane from different methanogenic pathways lack a systematic investigation. In this study, we provide a dataset encompassing the relative isotopologue abundances produced by hydrogenotrophic, methylotrophic, acetoclastic, and methoxydotrophic methanogenesis. We find that a statistical "combinatorial effect" generates significant differences in 12CH2D2 compositions between hydrogenotrophic methanogenesis and other pathways. The thermodynamic drive of methanogenic reactions and phylogenetic affiliation may also influence the isotope compositions of methane. Our study provides new experimental constraints on the isotope signatures of different microbial methanogenic pathways, and evidence of the mechanisms responsible for the observed differences. TeaserA novel stable isotope tool to track and differentiate sources of biological methane.

microbiology↗

bioRxiv2024

Neutrophil-chemoattractant CXCL5 induces lung barrier permeability in acute lung injury

RationaleAcute lung injury is frequently caused by pneumonia, and severity correlates with inflammatory cell recruitment and lung barrier failure. Deciphering drug-targetable pathways is of clinical importance. ObjectivesInvestigation of paracrine and autocrine effects of epithelial-derived chemokine CXCL5 in acute lung injury. MethodsWe assessed the role of CXCL5 and related chemokines in patients with severe pneumonia and primary cells or cell lines challenged with Streptococcus pneumoniae or exposed to mechanical stretch. Furthermore, we evaluated the role of CXCL5 in in vivo models of acute lung injury through use of Cxcl5-deficient mice and in vitro human lung barrier models. ResultsPneumococcal infection and mechanical ventilation were associated with CXCL5 production in human subjects and in mice. CXCL5 was produced by bronchial and alveolar epithelial cells. The alveolar-epithelial barrier was protected in acute lung injury models in Cxcl5-deficient mice, independent of alveolar neutrophil recruitment. Single-cell transcriptomics revealed enhanced cell junctional transcripts in epithelial, but not endothelial cells in Cxcl5-deficient mice. Accordingly, CXCL5 exposure disrupted the barrier function of TNF-primed human primary alveolar epithelial cells, but not pulmonary microvascular endothelial cells. ConclusionsWe describe a novel function of CXCL5 in acute lung injury. Besides its recognized role in recruiting highly inflammatory cells such as neutrophils, CXCL5 increases alveolar-epithelial barrier permeability. Thus, in severe bacterial pneumonia, targeting of CXCL5 as adjunctive therapy to antibiotics may aid in reducing overshooting inflammation as well as stabilizing lung barrier function.

immunology↗

bioRxiv2024

Non-random segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in daughter cells

The non-random segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial fission and fusion. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide the first in vivo evidence that the non-random segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division.

developmental biology↗

bioRxiv2024

Adult male Lar gibbon sings the female great-call: A case study of inter-sex song production in a non-human primate

Gibbons are known as one of the most vocal non-human primates. They vocally advertise and reinforce their pair-bonds by singing complex duets, in which both the male and female perform a predetermined sex-specific set of song phrases, including the loud and elongated great-calls. Only females and sub-adult male gibbons have been previously observed performing great-calls. Once a male gibbon matures, he normally stops great-call production completely but continues singing other and less high-pitched song phrases. This case study describes a fully adult, castrated male lar gibbon (Hylobates lar, 32 years old, zoo-housed) who performs both male phrases of the duet, including the female great-call. The male regularly produced great-calls despite being in a, relatively weak, pair bond with a female conspecific. His great-calls adhered to the general structure of typical female great-calls but were shorter and had a lower maximum frequency. Notably, he produced these great-calls predominantly when the female was absent, especially when she was in their inside enclosure whilst he was outside. Behavioural observations indicate that the occurrence of great-calls by the male cannot be predicted based on pre-song behaviour or his interaction with the female. The recurrence of sub-adult singing behaviour in a fully grown adult is most likely due to his reduced testosterone levels. This study sheds light on the intricate dynamics of duetting and the unique occurrence of cross-sex song production in gibbons, emphasizing the complexity of pair-bond communication in this species.

animal behavior and cognition↗

bioRxiv2024

Genome-wide profiling of highly similar paralogous genes using HiFi sequencing

Variant calling is hindered in segmental duplications by sequence homology. We developed Paraphase, a HiFi-based informatics method that resolves highly similar genes by phasing all haplotypes of a gene family. We applied Paraphase to 160 long (>10 kb) segmental duplication regions across the human genome with high (>99%) sequence similarity, encoding 316 genes. Analysis across five ancestral populations revealed highly variable copy numbers of these regions. We identified 23 families with exceptionally low within-family diversity, where extensive gene conversion and unequal-crossing over have resulted in highly similar gene copies. Furthermore, our analysis of 36 trios identified 7 de novo SNVs and 4 de novo gene conversion events, 2 of which are non-allelic. Finally, we summarized extensive genetic diversity in 9 medically relevant genes previously considered challenging to genotype. Paraphase provides a framework for resolving gene paralogs, enabling accurate testing in medically relevant genes and population-wide studies of previously inaccessible genes.

genomics↗

bioRxiv2024

Molecular Basis for RNA Cytidine Acetylation by NAT10

Human NAT10 acetylates the N4 position of cytidine in RNA, predominantly on rRNA and tRNA, to facilitate ribosome biogenesis and protein translation. NAT10 has been proposed as a therapeutic target in cancers as well as aging-associated pathologies such as Hutchinson-Gilford Progeria Syndrome (HGPS). The [~]120 kDa NAT10 protein uses its acetyl-CoA-dependent acetyltransferase, ATP-dependent helicase, and RNA binding domains in concert to mediate RNA-specific N4-cytidine acetylation. While the biochemical activity of NAT10 is well known, the molecular basis for catalysis of eukaryotic RNA acetylation remains relatively undefined. To provide molecular insights into the RNA-specific acetylation by NAT10, we determined the single particle cryo-EM structures of Chaetomium thermophilum NAT10 (CtNAT10) bound to a bisubstrate cytidine-CoA probe with and without ADP. The structures reveal that NAT10 forms a symmetrical heart-shaped dimer with conserved functional domains surrounding the acetyltransferase active sites harboring the cytidine-CoA probe. Structure-based mutagenesis with analysis of mutants in vitro supports the catalytic role of two conserved active site residues (His548 and Tyr549 in CtNAT10), and two basic patches, both proximal and distal to the active site for RNA-specific acetylation. Yeast complementation analyses and senescence assays in human cells also implicates NAT10 catalytic activity in yeast thermoadaptation and cellular senescence. Comparison of the NAT10 structure to protein lysine and N-terminal acetyltransferase enzymes reveals an unusually open active site suggesting that these enzymes have been evolutionarily tailored for RNA recognition and cytidine-specific acetylation.

biophysics↗

bioRxiv2024

Considerations for reporting variants in novel candidate genes identified during clinical genomic testing

Since the first novel gene discovery for a Mendelian condition was made via exome sequencing (ES), the rapid increase in the number of genes known to underlie Mendelian conditions coupled with the adoption of exome (and more recently, genome) sequencing by diagnostic testing labs has changed the landscape of genomic testing for rare disease. Specifically, many individuals suspected to have a Mendelian condition are now routinely offered clinical ES. This commonly results in a precise genetic diagnosis but frequently overlooks the identification of novel candidate genes. Such candidates are also less likely to be identified in the absence of large-scale gene discovery research programs. Accordingly, clinical laboratories have both the opportunity, and some might argue a responsibility, to contribute to novel gene discovery which should in turn increase the diagnostic yield for many conditions. However, clinical diagnostic laboratories must necessarily balance priorities for throughput, turnaround time, cost efficiency, clinician preferences, and regulatory constraints, and often do not have the infrastructure or resources to effectively participate in either clinical translational or basic genome science research efforts. For these and other reasons, many laboratories have historically refrained from broadly sharing potentially pathogenic variants in novel genes via networks like Matchmaker Exchange, much less reporting such results to ordering providers. Efforts to report such results are further complicated by a lack of guidelines for clinical reporting and interpretation of variants in novel candidate genes. Nevertheless, there are myriad benefits for many stakeholders, including patients/families, clinicians, researchers, if clinical laboratories systematically and routinely identify, share, and report novel candidate genes. To facilitate this change in practice, we developed criteria for triaging, sharing, and reporting novel candidate genes that are most likely to be promptly validated as underlying a Mendelian condition and translated to use in clinical settings.

genetics↗

bioRxiv2024

SIRT7 regulates NUCKS1 chromatin binding to elicit metabolic and inflammatory gene expression in senescence and liver aging

Sirtuins, a class of highly conserved histone/protein deacetylases, are heavily implicated in senescence and aging. The regulation of sirtuin proteins is tightly controlled both transcriptionally and translationally and via localization within the cell. While Sirtiun proteins are implicated with aging, how their levels are regulated during aging across cell types and eliciting tissue specific age-related cellular changes is unclear. Here, we demonstrate that SIRT7 is targeted for degradation during senescence and liver aging. To uncover the significance of SIRT7 loss, we performed proteomics analysis and identified a new SIRT7 interactor, the HMG box protein NUCKS1. We found that the NUCKS1 transcription factor is recruited onto chromatin during senescence and this is mediated by SIRT7 loss. Further, depletion of NUCKS1 delayed senescence upon DNA damage leading to reduction of inflammatory gene expression. Examination of NUCKS1 transcriptional regulation during senescence revealed gene targets of transcription factors NFKB1, RELA, and CEBP{beta}. Consistently, in both Sirt7 KO mouse liver and in naturally aged livers, Nucks1 was recruited to chromatin. Further, Nucks1 was bound at promoters and enhancers of age-related genes, including transcription factor Rela, and, moreover, these bound sites had increased accessibility during aging. Overall, our results uncover NUCKS1 as a novel interactor of SIRT7, and show that loss of SIRT7 during senescence and liver aging promotes NUCKS1 chromatin binding to regulate metabolic and inflammatory genes.

cell biology↗

bioRxiv2023

Low land-use intensity buffers grasslands against future climate and inter-annual climate variability in a large field experiment

Climate and land-use change are key drivers of global change. Full-factorial field experiments in which both drivers are manipulated are essential to understand and predict their potentially interactive effects on the structure and functioning of grassland ecosystems. Here, we present eight years of data on grassland dynamics from the Global Change Experimental Facility (GCEF) in Central Germany. On large experimental plots, temperature and seasonal patterns of precipitation are manipulated by superimposing regional climate model projections onto background climate variability. Climate manipulation is factorially crossed with agricultural land-use scenarios, including intensively used meadows and extensively used (i.e. low-intensity) meadows and pastures. Inter-annual variation of background climate during our study years was high, including three of the driest years on record for our region. The effects of this temporal variability far exceeded the effects of the experimentally imposed climate change on plant species diversity and productivity, especially in the intensively used, species-poor grasslands. These changes in productivity and diversity in response to alterations in climate were due to immigrant species replacing the target forage cultivars. This shift from forage cultivars to immigrant species may impose additional economic costs in terms of a decreasing fodder value and the need for more frequent management measures. In contrast, the extensively used, species-rich grasslands showed weaker responses to both experimentally manipulated future climate and inter-annual climate variability, suggesting that these diverse grasslands are more resistant to climate change than intensively used, species-poor grasslands. We therefore conclude that an extensive management of agricultural grasslands, together with other measures to increase species diversity, can stabilize primary productivity under climate change.

ecology↗

bioRxiv2023

Nutritional vitamin B12 regulates RAS/MAPK-mediated cell fate decisions through the one-carbon metabolism

Vitamin B12 is an essential nutritional co-factor for the folate and methionine cycles, which together constitute the one-carbon metabolism. Here, we show that dietary uptake of vitamin B12 modulates cell fate decisions controlled by the conserved RAS/MAPK signaling pathway in C. elegans. A bacterial diet rich in vitamin B12 increases vulval induction, germ cell apoptosis and oocyte differentiation. These effects are mediated by different one-carbon metabolites in a tissue-specific manner. Vitamin B12 enhances via the choline/phosphatidylcholine metabolism vulval induction by down-regulating fat biosynthesis genes and increasing H3K4 tri-methylation, which results in increased expression of RAS/MAPK target genes. Furthermore, the nucleotide metabolism and H3K4 tri-methylation positively regulate germ cell apoptosis and oocyte production. Using mammalian cells carrying different activated KRAS and BRAF alleles, we show that the effects of methionine on RAS/MAPK-regulated phenotype are conserved in mammals. Our findings suggest that the vitamin B12-dependent one-carbon metabolism is a limiting factor for diverse RAS/MAPK-induced cellular responses.

developmental biology↗

bioRxiv2023

Actomyosin-mediated apical constriction promotes physiological germ cell death in C. elegans

Germ cell apoptosis in C. elegans hermaphrodites is a physiological process eliminating around 60% of all cells in meiotic prophase to maintain tissue homeostasis. In contrast to programmed cell death in the C. elegans soma, the selection of germ cells undergoing apoptosis is stochastic. By live-tracking individual germ cells at the pachytene stage, we found that germ cells smaller than their neighbors are selectively eliminated through apoptosis before differentiating into oocytes. Thus, cell size is a strong predictor of physiological germ cell death. The RAS/MAPK and ECT/RHO/ROCK pathways together regulate germ cell size by controlling actomyosin constriction at the apical rachis bridges, which are cellular openings connecting the syncytial germ cells to a shared cytoplasmic core. Enhancing apical constriction reduces germ cell size and increases the rate of cell death while inhibiting the actomyosin network in the germ cells prevents their death. We propose that actomyosin contractility at the rachis bridges of the syncytial germ cells amplifies intrinsic disparities in cell size. Through this mechanism, animals can adapt the rate of germ cell death and differentiation to changing environmental conditions.

developmental biology↗