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A multiscale analysis of early flower development in Arabidopsis provides an integrated view of molecular regulation and growth control

The link between gene regulation and morphogenesis of multicellular organisms is a fundamental problem in biology. We address this question in the floral meristem of Arabidopsis, which generates new tissues and organs through complex changes in growth patterns. Starting from high-resolution time-lapse images, we generated a comprehensive 4-D atlas of early flower development including cell lineage, cellular growth rates and the expression patterns of 28 regulatory genes. This information was introduced in MorphoNet, a web-based open-access platform. The application of mechanistic computational models indicated that the molecular network based on the literature only explained a minority of the expression patterns. This was substantially improved by adding single regulatory hypotheses for individual genes. We next used the integrated information to correlate growth with the combinatorial expression of multiple genes. This led us to propose a set of hypotheses for the action of individual genes in morphogenesis, not visible by simply correlating gene expression and growth. This identified the central transcription factor LEAFY as a potential regulator of heterogeneous growth, which was supported by quantifying growth patterns in a leafy mutant. By providing an integrated, multiscale view of flower development, this atlas should represent a fundamental step towards mechanistic multiscale-scale models of flower development.

developmental biology↗

Towards identifying subnetworks from FBF binding landscapes in Caenorhabditis spermatogenic or oogenic germlines

Metazoan PUF (Pumilio and FBF) RNA-binding proteins regulate various biological processes, but a common theme across phylogeny is stem cell regulation. In Caenorhabditis elegans, FBF (fem-3 Binding Factor) maintains germline stem cells regardless of which gamete is made, but FBF also functions in the process of spermatogenesis. We have begun to \"disentangle\" these biological roles by asking which FBF targets are gamete-independent, as expected for stem cells, and which are gamete-specific. Specifically, we compared FBF iCLIP binding profiles in adults making sperm to those making oocytes. Normally, XX adults make oocytes. To generate XX adults making sperm, we used a fem-3(gf) mutant requiring growth at 25{degrees}; for comparison, wild-type oogenic hermaphrodites were also raised at 25{degrees}. Our FBF iCLIP data revealed FBF binding sites in 1522 RNAs from oogenic adults and 1704 RNAs from spermatogenic adults. More than half of these FBF targets were independent of germline gender. We next clustered RNAs by FBF-RNA complex frequencies and found four distinct blocks. Block I RNAs were enriched in spermatogenic germlines, and included validated target fog-3, while Block II and III RNAs were common to both genders, and Block IV RNAs were enriched in oogenic germlines. Block II (510 RNAs) included almost all validated FBF targets and was enriched for cell cycle regulators. Block III (21 RNAs) was enriched for RNA-binding proteins, including previously validated FBF targets gld-1 and htp-1. We suggest that Block I RNAs belong to the FBF network for spermatogenesis, and that Blocks II and III are associated with stem cell functions.

developmental biology↗

Noncanonical Wnt/Ror2 Signaling Regulates Basal Cell Fidelity and Branching Morphogenesis in the Mammary Gland

The mammary gland epithelium relies on a delicate balance between basal and luminal cell lineages to maintain tissue homeostasis and enable proper development. While the role of canonical Wnt signaling in mammary biology is well-established, the contribution of noncanonical Wnt signaling to lineage identity has remained unclear. Noncanonical Wnt pathways are primarily associated with morphogenesis, cytoskeletal regulation, and cell migration, but whether they are required for maintaining epithelial cell fate remains largely unexplored. Here, we demonstrate that the noncanonical Wnt receptor Ror2 is expressed in both basal and luminal lineages, yet selectively maintained in basal cells throughout development, suggesting a lineage-specific function. Using a p63CreERT2/+ lineage-specific mouse model, we show that Ror2 deletion in basal epithelial cells enhances secondary and tertiary branching while driving a basal-to-luminal fate transition, marked by downregulation of basal markers (K14, K5) and upregulation of luminal markers (K8, K18, ER). Mechanistically, Ror2 loss disrupts RhoA-ROCK1-YAP1 signaling, leading to cytoskeletal reorganization, chromatin remodeling, and increased accessibility at luminal regulatory loci. Notably, ROCK1 inhibition phenocopies Ror2 loss, reinforcing the critical role of the RhoA-ROCK1 axis in basal cell maintenance. These findings provide direct genetic and mechanistic evidence that noncanonical Wnt signaling is essential for maintaining basal lineage fidelity, offering new insights into the mechanisms regulating epithelial plasticity. Given the fundamental importance of lineage stability in epithelial homeostasis, our results suggest that disruptions in Wnt/Ror2 signaling may contribute to aberrant fate transitions relevant to breast cancer progression.

developmental biology↗

20-hydroxyecdysone (20E) signaling regulates amnioserosa morphogenesis during Drosophila dorsal closure: Ecdysone receptor modulates gene expression in a complex with the AP-1 component, Jun

Steroid hormones influence diverse biological processes throughout the animal life cycle, including metabolism, stress resistance, reproduction, and lifespan. In insects, the steroid hormone, 20-hydroxyecdysone (20E), is the central regulator of molting and metamorphosis, and has been shown to play roles in tissue morphogenesis. For example, amnioserosa contraction, which is a major driving force in Drosophila dorsal closure (DC), is defective in embryos mutant for 20E biosynthesis. Here, we show that 20E signaling modulates the transcription of several DC participants in the amnioserosa and other dorsal tissues during late embryonic development, including the zipper locus, which encodes for non-muscle myosin II heavy chain. Canonical 20E signaling typically involves the binding of Ecdysone receptor (EcR) and Ultraspiracle heterodimers to ecdysone-response elements (EcREs) within the promoters of ecdysone-responsive genes to drive their expression. During DC, we provide evidence that 20E signaling instead acts in parallel to the JNK cascade via a direct interaction between EcR and the AP-1 component, Jun, which together binds to genomic regions containing AP-1 binding sites but no EcREs to control gene expression. Our work demonstrates a novel mode of action for 20E signaling in Drosophila that likely functions beyond DC, and may provide further insights into mammalian steroid hormone receptor interactions with AP-1.

developmental biology↗

Discovery of a new craniofacial gene influencing adaptive phenotypes in a non-model pupfish radiation

Understanding the genetic basis of novel adaptations in new species is a fundamental question in biology that also provides an opportunity to uncover new genes and regulatory networks with potential clinical relevance. Here we demonstrate a new role for galr2 in vertebrate craniofacial development using an adaptive radiation of trophic specialist pupfishes endemic to San Salvador Island in the Bahamas. We confirmed the loss of a putative Sry transcription factor binding site in the upstream region of galr2 in scale-eating pupfish and found significant spatial differences in galr2 expression among pupfish species in Meckels cartilage and premaxilla using in situ hybridization chain reaction (HCR). We then experimentally demonstrated a novel function for Galr2 in craniofacial development and jaw elongation by exposing embryos to drugs that inhibit Galr2 activity. Galr2-inhibition reduced Meckels cartilage length and increased chondrocyte density in both trophic specialists but not in the generalist genetic background. We propose a mechanism for jaw elongation in scale-eaters based on the reduced expression of galr2 due to the loss of a putative Sry binding site. Fewer Galr2 receptors in the scale-eater Meckels cartilage may result in their enlarged jaw lengths as adults by limiting opportunities for a postulated Galr2 agonist to bind to these receptors during development. Our findings illustrate the growing utility of linking candidate adaptive SNPs in non-model systems with highly divergent phenotypes to novel vertebrate gene functions.

developmental biology↗

In vitro sexual dimorphism establishment in schistosomes

Schistosomes are parasitic flatworms that cause Schistosomiasis, a major Neglected Tropical Disease (NTD) that affects more than 250 million people worldwide. With two morphologically distinct sexes, a heterogametic female (ZW) and a homogametic male (ZZ), schistosomes are an exception among flatworms, which are largely hermaphroditic. Sexual dimorphism in schistosomes only becomes apparent by adulthood within the mammalian host. The cellular and molecular mechanisms underlying the sexual differentiation of these parasites are poorly understood, partly due to intrinsic challenges in assessing parasite development in vivo. Therefore, robust and reproducible approaches for maintaining and developing parasites in vitro are needed to overcome these difficulties. However, to date, only a few studies have focused on protocols that allow cultured parasites to reach sexual dimorphic stages, and none have been reproduced, limiting the ability to understand the unique sexual biology of this major human parasite. Here, we refine a protocol for long-term culture of newly transformed cercariae that developed in vitro into sexually dimorphic forms. We assessed the effect of two different sera, Foetal Bovine Serum (FBS) and Human Serum (HS), added to the culture medium supplemented with human red blood cells. We found that in contrast to FBS-cultured worms, HS-cultured parasites digested red blood cells, a crucial step for long term parasite development. Additionally, while most FBS-cultured parasites did not progress beyond an early liver stage, sexual dimorphism was clearly established in the HS-cultured worms, albeit delayed compared to in vivo development. Moreover, EdU pulse experiments revealed a continuous proliferation of cells over time in HS-cultured parasites, while a significantly lower number of proliferating cells were detected in FBS-cultured worms. This protocol paves the way to study parasite development in vitro, positively impacting the principles of the 3Rs (Replacement, Reduction and Refinement) for animal research, and allowing for in-depth studies of sexual dimorphism establishment as well as in vitro screening for novel control strategies across the life cycle of these major human parasites.

developmental biology↗

Highly efficient tamoxifen-inducible Cre recombination in embryonic, larval and adult zebrafish

We have generated transgenic lines containing zebrafish-optimized CreERT2 recombinase under the control of a recombinant ubbR promoter consisting of the zebrafish ubiquitin promoter supplemented with an intronic enhancer from the carp beta-actin2 gene. These lines enable highly efficient tamoxifen-inducible recombination in embryonic, larval and adult zebrafish. AbstractThe ability to inactivate gene function in an adult organism is essential for studies of biological processes such as regeneration and behavior. This is best achieved by engineering an allele which could be conditionally inactivated using Cre recombinase and subsequently inactivating gene function using a drug-inducible Cre recombinase. Several recent studies clearly demonstrate feasibility of engineering such conditional alleles in zebrafish. Meanwhile, achieving sufficient degree of recombination to induce complete loss of function has remained a major limitation. Herein we address this limitation by engineering a recombinant ubiquitin promoter ubbR consisting of the zebrafish ubiquitin promoter supplemented with an intronic enhancer from the carp beta-actin2 gene. Using phiC31-mediated targeted integration, we demonstrate that ubbR clearly outperforms both parental promoters as well as currently available ubiquitous CreERT2 driver lines at all embryonic and larval stages tested. Furthermore, the ubbR:CreERT2driver line we generated enables near-complete inactivation of floxed alleles in adult zebrafish hearts. Finally, we demonstrate that our ubbRpromoter retains high activity when integrated at other genomic loci, making it uniquely suitable for robust expression of transgenes at all stages of zebrafish ontogenesis. HighlightsO_LIUsed targeted integration to directly compare different CreERT2 drivers C_LIO_LIGenerated a ubiquitous ubbR:CreERT2 driver line capable of near-complete inactivation of floxed genes in adult zebrafish hearts C_LIO_LIDemonstrated that the recombinant ubbR promoter is suitable for robust transgene expression when integrated at different genomic loci C_LI

developmental biology↗

Monsters in the uterus: A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

Many diseases whose frequency increases with advancing age are caused by aging (senescence), but the mechanisms of senescence remain poorly understood. According to G.C. Williams and M.V. Blagosklonny, a major etiological determinant of senescence is late-life, wild-type gene action and non-adaptive execution of biological programs (or quasi-programs). These generate a wide range of senescent pathologies causing illness and death. Here we investigate the etiology of a prominent senescent pathology in the nematode C. elegans, uterine tumors, in the light of the Williams Blagosklonny theory. Uterine tumors develop from unfertilized, immature oocytes which execute incomplete embryogenetic programs. This includes extensive endomitosis, leading to formation of chromatin masses and cellular hypertrophy. The starting point of pathogenesis is exhaustion of sperm stocks. The timing of this transition between program and quasi-program can be altered by blocking sperm production (causing earlier tumors) or supplying additional sperm by mating (delaying tumor onset). Other pathophysiological determinants are yolk consumption by tumors, and bacterial proliferation within tumors. Uterine tumors resemble mammalian ovarian teratomas (tera, Greek: monster) in that both develop from oocytes that fail to mature after meiosis I, and both are the result of quasi-programs. Moreover, older but not younger uterine tumors show expression of markers of later embryogenesis, i.e. are teratoma-like. These results show how uterine tumors in C. elegans form as the result of run-on of embryogenetic quasi-programs. They also suggest fundamental etiological equivalence between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

developmental biology↗

Different cellular and molecular mechanisms of chitin deposition contribute to the specificity of the two chitin synthases in D. melanogaster.

Chitin is a major component of arthropod extracellular matrices, including the exoskeleton and the midgut peritrophic matrix. It plays a key role in the development, growth and viability of insects. Besides the biological importance of this aminopolysaccharide, chitin also receives a lot of attention for its practical applications in medicine and biotechnology as a superior biopolymer with excellent physicochemical and mechanical properties. Chitin is produced and deposited extracellularly by chitin synthases. Most insects encode two types of chitin synthases, presumably with type A being required for exoskeletons and type B to produce the peritrophic matrix. It is not fully understood, however, which factors contribute to the specificity of each type of chitin synthase. Here we leverage the advantages of Drosophila melanogaster for functional manipulations to evaluate the mechanisms of activity and functional requirements of Kkv (Chitin synthase A) and Chs2 (Chitin synthase B). We first demonstrate that Chs2 is expressed and required in a region in the larval proventriculus that produces the chitin deposited in the peritrophic matrix. We then analyse whether the two chitin synthases can replace each other. We also investigate the subcellular localisation of these chitin synthases in different tissues and their ability to deposit chitin in combination with known auxiliary proteins. Our results indicate that the two different chitin synthases are not functionally equivalent, and that they use specific cellular and molecular mechanisms to deposit chitin. We suggest that the specificity of the different insect chitin synthases may underly the production of chitin polymers with different properties, conferring different physiological activities to the extracellular matrices.

developmental biology↗

Endophyte Chaetomium globosum D38 and its elicitors promote tanshinones accumulation of Salvia miltiorrhiza

Due to the low yield of tanshinones and their analogues in Salvia miltiorrhiza, there are all kinds of stimulation strategies having been applied to improve tanshinones output in plant tissue cultures. Endophytic fungi have formed various different relationships with their host plants withstanding host and environmental factors, including symbiotic, mutualistic, commensalistic, and parasitic. Thus we take the assumption that endophytic fungi may be an emerging microbial tool used to promote secondary metabolism, which will promote the production of active compounds through endophyte-based biology method. Our study therefore aimed to examine the effects of live endophytic fungus Chaetomium globosum D38 and its elicitors on the accumulation of tanshinones in hairy root cultures of Salvia miltiorrhiza. C. globosum D38 mainly colonized in the intercellular gap of xylem parenchyma cells of S. miltiorrhiza hairy root, during long term co-existence without any toxicity against S. miltiorrhiza hairy root. Moreover, both of the live fungus and its mycelia extracts could induce the production of tanshinones, in special dihydrotanshinone I and cryptotanshinone. The effects of mycelia extracts were much stronger than that of the live fungus on tanshinones synthesis, which increased the transcriptional activity of genes with repect to tanshinone biosynthetic pathway obviously. Our results indicated that both of the live C. globosum D38 and its mycelia extracts could be utilized for tanshinones accumulation in S. miltiorrhiza hairy root. Whats more, D38 also could be made into biotic fertilizer applying into S.miltiorrhiza seddlings, which not only promoted host growth but the tanshinones and phenylpropionic acid accumulation. In the soil environment, D38 had formed bitrophic and mutual beneficial relationship with the host and enhanced the primary metabolism on the whole so as to have facilitative effects on phenylpropionic acid accumulation. To sum up, Chaetomium globosum D38 was a highly effective endophytic fungus for S. miltiorrhiza.

developmental biology↗

Combining Stem Cell Rejuvenation and Senescence Targeting to Synergistically Extend Lifespan

Why biological age is a major risk factor for many of the most important human diseases remains mysterious. We know that as organisms age, stem cell pools are exhausted while senescent cells progressively accumulate. Independently, induction of pluripotency via expression of Yamanaka factors (Oct4, Klf4, Sox2, c-Myc; OKSM) and clearance of senescent cells have each been shown to ameliorate cellular and physiological aspects of aging, suggesting that both processes are drivers of organismal aging. However, stem cell exhaustion and cellular senescence likely interact in the etiology and progression of age-dependent diseases because both undermine tissue and organ homeostasis in different if not complementary ways. Here, we combine transient cellular reprogramming (stem cell rejuvenation) with targeted removal of senescent cells to test the hypothesis that simultaneously targeting both cell-fate based aging mechanisms will maximize life and health span benefits. We show that these interventions protect the intestinal stem cell pool, lower inflammation, activate pro-stem cell signaling pathways, and synergistically improve health and lifespan. Our findings suggest that a combination therapy, simultaneously replacing lost stem cells and removing senescent cells, shows synergistic potential for anti-aging treatments. Our finding that transient expression of both is the most effective suggests that drug-based treatments in non-genetically tractable organisms will likely be the most translatable.

developmental biology↗

Mood variability during adolescent development and their relation to sleep and brain development

Mood swings, or mood variability, are associated with negative mental health outcomes. Since adolescence is a time when mood disorder onset peaks, mood variability during this time is of significant interest. Understanding biological factors that might be associated with mood variability, such as sleep and structural brain development, could elucidate the mechanisms underlying mood and anxiety disorders. Data from the longitudinal Leiden Self-Concept study (N=171) over 5 yearly timepoints was used to study the association between sleep, brain structure, and mood variability in healthy adolescents aged 11-21 at baseline in this pre-registered study. Sleep was measured both objectively, using actigraphy, as well as subjectively, using a daily diary self-report. Negative mood variability was defined as day-to-day negative mood swings over a period of 5 days after an MRI scan. It was found that negative mood variability peaked in mid-adolescence in females while it linearly increased in males, and average negative mood showed a similar pattern. Sleep duration (subjective and objective) generally decreased throughout adolescence, with a larger decrease in males. Mood variability was not associated with sleep, but average negative mood was associated with lower self-reported energy. In addition, higher thickness in the dorsolateral prefrontal cortex (dlPFC) compared to same-age peers, suggesting a delayed thinning process, was associated with higher negative mood variability in early and mid-adolescence. Together, this study provides an insight into the development of mood variability and its association with brain structure.

developmental biology↗

KK-LC-1 reveals evolutionary divergence in the regulation of sperm motility between humans and mice

CT83 (KK-LC-1) is a cancer-testis antigen originally identified in human lung cancer cells and has recently attracted attention as a potential target for cancer therapy. Although KK-LC-1 orthologs have been identified in up to 160 animal species, a murine homolog had not previously been identified, hindering in vivo analysis of its physiological function. In this study, we identified the mouse homolog of KK-LC-1 and performed a comparative analysis of its properties in humans and mice, together with an investigation of its biological function using gene knockout (KO) mice. The murine Kk-lc-1 gene is located on the X chromosome and, like its human counterpart, contains an N-terminal transmembrane domain. In both humans and mice, KK-LC-1 is expressed specifically in the testis and localizes to the head and tail regions of sperm. Analysis of Kk-lc-1-deficient mice revealed normal spermatogenesis, and both male and female KO mice were fertile. However, sperm from Kk-lc-1-deficient males exhibited reduced motility caused by decreased flexibility of the midpiece and failed to penetrate the oocyte zona pellucida in vitro. This defect was rescued by artificial insemination using epididymal sperm, suggesting that maternal factors in vivo may compensate for reduced sperm motility. Although impaired sperm motility during in vitro fertilization (IVF) was rescued by murine Kk-lc-1, functional rescue by human KK-LC-1 was not observed. These findings indicate that KK-LC-1 contributes to sperm motility but is not essential for fertility. Moreover, species-specific differences in KK-LC-1-mediated regulation of sperm motility suggest functional divergence during evolution. The role of KK-LC-1 in sperm motility should therefore be considered in the clinical development of cancer therapies targeting KK-LC-1.

developmental biology↗

Shining stars: Transgenesis and efficient metamorphosis in the sea star Patiria miniata

The sea star Patiria miniata is a widely used and powerful model organism for cell, developmental, and reproductive biology, but it has lacked genetic tools for expressing transgenes or endogenously tagging proteins. We developed a protocol to endogenously tag a broadly expressed actin gene and to express additional fluorescent markers from the same locus, using CRISPR/Cas9 genome editing. We also identified and isolated a promoter sequence of this actin gene which drives expression of transgenes. This promoter and transgene cassette can be introduced via a plasmid into the genome and persist through metamorphosis into the juvenile stage. Robust methods to induce metamorphosis that result in healthy juveniles are essential for developing stable transgenic lines and have been lacking in the field. Here we report a fast and efficient approach to induce the metamorphosis of larvae into healthy juveniles by introducing surf clam shells. Thus, we present a reliable method to generate both CRISPR/Cas9 knock-in and plasmid-integrated transgenic juvenile P. miniata, enabling future research on their fascinating biology, including regeneration, oogonial stem cells, metamorphosis, and more.

developmental biology↗

Evidence that Runt Acts as a Counter-Repressor of Groucho during Drosophila melanogaster Primary Sex Determination

Runx proteins are bifunctional transcription factors that both repress and activate transcription in animal cells. Typically Runx proteins work in concert with other transcriptional regulators, including co-activators and co-repressors to mediate their biological effects. In Drosophila melanogaster the archetypal Runx protein, Runt, functions in numerous processes including segmentation, neurogenesis and sex determination. During primary sex determination Runt acts as one of four X-linked signal element (XSE) proteins that direct female-specific activation of the establishmen promoter (Pe) of the master regulatory gene Sex-lethal (Sxl). Successful activation of SxlPe requires that the XSE proteins overcome the repressive effects of maternally deposited Groucho (Gro), a potent co-repressor of the Gro/TLE family. Runx proteins, including Runt, contain a C-terminal peptide, VWRPY, known to bind to Gro/TLE proteins to mediate transcriptional repression. We show that Runts VWRPY co-repressor-interaction domain is needed for Runt to activate SxlPe. Deletion of the Gro-interaction domain eliminates Runt-ability to activate SxlPe, whereas replacement with a higher affinity, VWRPW, sequence promotes Runt-mediated transcription. This suggest that Runt activates SxlPe by antagonizing Gro function, a conclusion consist with earlier findings that Runt is needed for Sxl expression only in embryonic regions with high Gro activity. Surprisingly we found that Runt is not required for the initial activation activation of SxlPe. Instead, Runt is needed to keep SxlPe active during the subsequent period of high-level Sxl transcription suggesting that Runt helps amplfy the difference between female and male XSE signals by counterrepressing Gro in female, but not in male, embryos.

developmental biology↗

Statistical description of mobile oscillators in embryonic pattern formation

Synchronization of mobile oscillators occurs in numerous contexts, including physical, chemical, biological and engineered systems. In vertebrate embryonic development, a segmental body structure is generated by a population of mobile oscillators. Cells in this population produce autonomous gene expression rhythms, and interact with their neighbors through local signaling. These cells form an extended tissue where frequency and cell mobility gradients coexist. Gene expression kinematic waves travel through this tissue and pattern the segment boundaries. It has been shown that oscillator mobility promotes global synchronization. However, in vertebrate segment formation, mobility may also introduce local fluctuations in kinematic waves and impair segment boundaries. Here we derive a general framework for mobile oscillators that relates local mobility fluctuations to synchronization dynamics and pattern robustness. We formulate a statistical description of mobile phase oscillators in terms of a probability density. We obtain and solve diffusion equations for the average phase and variance, revealing the relationship between local fluctuations and global synchronization in a homogeneous population of oscillators. Analysis of the probability density for large mobility identifies a mean-field transition, where locally coupled oscillators start behaving as if each oscillator was coupled with all the others. We extend the statistical description to inhomogeneous systems to address the gradients present in the vertebrate segmenting tissue. The theory relates pattern stability to mobility, coupling and pattern wavelength. The general approach of the statistical description may be applied to mobile oscillators in other contexts, as well as to other patterning systems where mobility is present.

developmental biology↗

A systems biology approach uncovers the core gene regulatory network governing iridophore fate choice from the neural crest.

Multipotent neural crest (NC) progenitors generate an astonishing array of derivatives, including neuronal, skeletal components and pigment cells (chromatophores), but the molecular mechanisms allowing balanced selection of each fate remain unknown. In zebrafish, melanocytes, iridophores and xanthophores, the three chromatophore lineages, are thought to share progenitors and so lend themselves to investigating the complex gene regulatory networks (GRNs) underlying fate segregation of NC progenitors. Although the core GRN governing melanocyte specification has been previously established, those guiding iridophore and xanthophore development remain elusive. Here we focus on the iridophore GRN, where mutant phenotypes identify the transcription factors Sox10, Tfec and Mitfa and the receptor tyrosine kinase, Ltk, as key players. We present expression data, as well as loss and gain of function results, guiding the derivation of an initial iridophore specification GRN. Moreover, we use an iterative process of mathematical modelling, supplemented with a novel, Monte Carlo screening algorithm suited to the qualitative nature of the experimental data, to allow for rigorous predictive exploration of the GRN dynamics. Predictions were experimentally evaluated and testable hypotheses were derived to construct an improved version of the GRN, which we showed produced outputs consistent with experimentally observed gene expression dynamics. Our study reveals multiple important regulatory features, notably a sox10-dependent positive feedback loop between tfec and ltk driving iridophore specification; the molecular basis of sox10 maintenance throughout iridophore development; and the cooperation between sox10 and tfec in driving expression of pnp4a, a key differentiation gene. We also assess a candidate repressor of mitfa, a melanocyte-specific target of sox10. Surprisingly, our data challenge the reported role of Foxd3, an established mitfa repressor, in iridophore regulation. Our study builds upon our previous systems biology approach, by incorporating physiologically-relevant parameter values and rigorous evaluation of parameter values within a qualitative data framework, to establish for the first time the core GRN guiding specification of the iridophore lineage.\n\nAuthor SummaryMultipotent neural crest (NC) progenitors generate an astonishing array of derivatives, including neuronal, skeletal components and pigment cells, but the molecular mechanisms allowing balanced selection of each fate remain unknown. In zebrafish, melanocytes, iridophores and xanthophores, the three chromatophore lineages, are thought to share progenitors and so lend themselves to investigating the complex gene regulatory networks (GRNs) underlying fate segregation of NC progenitors. Although the core GRN governing melanocyte specification has been previously established, those guiding iridophore and xanthophore development remain elusive. Here we present expression data, as well as loss and gain of function results, guiding the derivation of a core iridophore specification GRN. Moreover, we use a process of mathematical modelling and rigorous computational exploration of the GRN to predict gene expression dynamics, assessing them by criteria suited to the qualitative nature of our current understanding of iridophore development. Predictions were experimentally evaluated and testable hypotheses were derived to construct an improved version of the GRN, which we showed produced outputs consistent with experimentally observed gene expression dynamics. The core iridophore GRN defined here is a key stepping stone towards exploring how chromatophores fate decisions are made in multipotent NC progenitors.

developmental biology↗

Differential proliferation regulates multi-tissue morphogenesis during embryonic axial extension: Integrating viscous modeling and experimental approaches.

The study of how mechanical interactions and different cellular behaviors affect tissues and embryo shaping has been and remains an important challenge in biology. Axial extension is a morphogenetic process that results in the acquisition of the elongated shape of the vertebrate embryonic body. Several adjacent tissues are involved in the process, including the tissues that form the spinal cord and musculoskeletal system: the neural tube and the paraxial mesoderm, respectively. Although we have a growing understanding of how each of these tissues elongates, we still need to fully understand the morphogenetic consequences of their growth and mechanical interactions. In this study, we develop a 2D multi-tissue continuum-based mathematical model to simulate and study how differential growth, tissue biophysical properties, and mechanical interactions affect the morphogenesis of the embryonic body during axial extension. Our model captures the long-term dynamics of embryonic posterior tissues previously observed in vivo by time-lapse imaging of bird embryos. It reveals the underestimated influence of differential tissue proliferation rates in inter-tissue interaction and shaping by capturing the relative impact of this process on tissue dynamics. We verified the predictions of our model in quail embryos by showing that decreasing the rate of cell proliferation in the paraxial mesoderm affects long-term tissue dynamics and shaping of both the paraxial mesoderm and the neighboring neural tube. Overall, our work provides a new theoretical platform to consider the long-term consequences of tissue differential growth and mechanical interactions on morphogenesis.

developmental biology↗