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Results for “developmental biology”

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bioRxiv2022

GPCR Signaling Promotes a Stress-induced Genetic Program for Phenoptosis in C. elegans

How an organism dies is a fundamental yet poorly understood question in biology. An organism can die of many causes, including stress-induced phenoptosis, also defined as organismic death that is regulated by its genome-encoded programs. The mechanism of stress-induced phenoptosis is still largely unknown. Here we show that transient but severe freezing-thaw stress (FTS) in C. elegans induces rapid and robust phenoptosis that is regulated by G-protein coupled receptor (GPCR) signaling. RNAi screens identify the GPCR-encoding fshr-1 in mediating transcriptional responses to FTS. FSHR-1 increases ligand interaction upon FTS and activates a cyclic AMP-PKA cascade leading to a genetic program to promote organismic death under severe stress. FSHR-1/GPCR signaling up-regulates the bZIP-type transcription factor ZIP-10, linking FTS to expression of genes involved in lipid remodeling, proteostasis and aging. A mathematical model suggests that genes may promote organismic death under severe stress conditions, potentially benefiting growth of the clonal population with individuals less stressed and more reproductively privileged. Our studies reveal roles of FSHR-1/GPCR-mediated signaling in stress-induced gene expression and phenoptosis in C. elegans, providing empirical new insights into mechanisms of stress-induced phenoptosis with evolutionary implications.

developmental biology↗

bioRxiv2020

Zfp36l1 and Zfp36l2 balances proliferation and differentiation in the developing retina

Both transcriptional and post-transcriptional regulation of gene expression play significant roles in diverse biological processes, but little is known about how post-transcriptional regulation impacts retinal development. Here we report our study of the function of two members of the TTP (tristetraprolin) mRNA binding protein family, Zfp36l1 and Zfp36l2, in the developing retina. TTP proteins are highly conserved CCCH zinc finger proteins, which carry out their functions by promoting target mRNA decay and modulating translation. We found that Zfp36l1 and Zfp36l2 were expressed in retinal progenitor cells (RPCs) during development and Muller glial cells and photoreceptors in the mature retina. Our analysis of the mutant retinas showed that, whereas the single knockout retinas were largely normal, the double knockout (DKO) retina showed decreased RPC proliferation and increased differentiation of multiple retinal cell types. RNA-seq analysis confirmed the imbalance of proliferation and differentiation in the DKO retina. Gene ontology and in silico target gene analysis indicates that Zfp36l1 and Zfp36l2 exert their function by directly regulating multiple classes of proteins, including components of multiple signaling pathways such as the sonic hedgehog pathway and the Notch pathway, cell cycle regulators, and most interestingly transcription factors directly involved in retinal differentiation. These results reveal a new tier of gene regulation controlling retinal development.

developmental biology↗

bioRxiv2020

Ets2 frame-shift mutant models express in-frame mRNA by exon skipping that complements Ets2 function in the skin

The Ets2 transcription factor has been implicated in various biological processes. An Ets2 mutant model, which lacks the DNA-binding domain (ETS domain), was previously reported to exhibit embryonic lethality caused by a trophoblast abnormality. This phenotype could be rescued by tetraploid complementation, resulting in pups with wavy hair. Here, we generated new Ets2 mutant models with deletions in exon 8 and with frame-shift mutations using the CRISPR/Cas9 method. Homozygous mutants could not be obtained by natural mating as previously reported. After rescuing with tetraploid complementation, homozygous mutant mice were generated, but these mice did not exhibit wavy hair phenotype. Our newly generated mice exhibited exon 8 skipping, which led to in-frame mutant mRNA expression in the skin and thymus but not in E7.5 embryos. As this in-frame mutation contained the ETS domain, the exon 8-skipped Ets2 mRNA was likely translated into protein in the skin that complemented the Ets2 function. Thus, these Ets2 mutant models, depending on the cell types, exhibited novel phenotypes due to exon skipping and are expected to be useful in several fields of research. Summary statementNew Ets2 mutant models showed embryonic lethal phenotype by a placental abnormality but did not exhibit a wavy hair phenotype as a previous model.

developmental biology↗

bioRxiv2021

Dynamic profiling and functional interpretation of histone lysine crotonylation and lactylation during neural development

BackgroundMetabolites such as crotonyl-CoA and lactyl-CoA influence gene expression through covalently modifying histones, known as histone lysine crotonylation (Kcr) and histone lysine lactylation (Kla). However, their existence patterns, dynamic changes, biological functions, as well as associations with histone lysine acetylation (Kac) and gene expression during mammalian development remain largely unknown, which imped us from understanding the epigenetic regulations of histone lysine acylations. ResultsHistone Kcr and Kla are widely distributed and undergo global changes during neural development. By profiling genome-wide dynamics of H3K9ac, H3K9cr and H3K18la in combination with ATAC sequencing and RNA sequencing, we reveal that these histone marks cooperatively regulate chromatin state and gene expression, as well as promote transcriptome remodelling to favour cell fate transition in the developing telencephalon. Importantly, we demonstrate that global histone Kcr and Kla are not consequence of transcription and furtherly identify histone deacetylase 1-3 (HDAC1-3) as novel "erasers" of H3K18la. Taking advantage of induced differentiation system of P19 embryonal carcinoma (EC) cells, we find that a selective inhibitor of HDAC1-3, MS-275 pre-activates neural fate-related transcriptional programs via stimulating multiple histone lysine acylations simultaneously. ConclusionsOur study uncover the interplays between histone lysine acylations to regulate gene expression and the differentiation-promoting functions of histone Kcr and Kla during development, and provide evidence that multiple histone lysine actlations synchronously alternate to orchestrate transcriptome responding under HDACs inhibition.

developmental biology↗

bioRxiv2020

Analysis of socioeconomic disadvantage and pace of aging measured in saliva DNA methylation of children and adolescents

Children who grow up in socioeconomically disadvantaged families face increased burden of disease and disability as they mature into adulthood. One hypothesized mechanism for this increased burden is that early-life disadvantage and its associated psychological stress accelerate biological processes of aging, increasing vulnerability to subsequent disease. In order to evaluate this hypothesis and the potential impact of preventive interventions, measures to quantify the early acceleration of biological aging in childhood are needed. Here, we evaluated a novel DNA-methylation measure of the pace of aging, DunedinPoAm, and compared DunedinPoAm results with results for several published epigenetic clocks. Data on saliva DNA-methylation and socioeconomic circumstances were collected from N = 600 children and adolescents aged 8- to 18-years-old (48% female) participating in the Texas Twin Project. Participants living in more disadvantaged families and neighborhoods exhibited faster pace of aging (r = 0.18, p = 0.001 for both). Latinx-identifying children exhibited faster DunedinPoAm compared to both White- and Latinx-White-identifying children, consistent with higher levels of disadvantage in this group. Children with more advanced pubertal development and those with had higher body-mass index also exhibited faster DunedinPoAm, but these covariates did not account for the observed socioeconomic gradient in methylation pace of aging. In contrast to findings for DunedinPoAm, we did not detect associations of socioeconomic disadvantage with five published epigenetic clocks. Findings suggest that DNA-methylation pace-of-aging measures may prove more sensitive to health damaging effects of adversity, particularly when measurements are taken early in the life course, before substantial aging has occurred.

developmental biology↗

bioRxiv2018

Distinct Sources of a Bovine Blastocyst Digital Image do not Produce the Same Classification by a Previously Trained Software using Artificial Neural Network

We develop an online graphical and intuitive interface connected to a server aiming to facilitate access to professionals worldwide that face problems with bovine blastocysts classification. The interface Blasto3Q (3Q is referred to the three qualities of the blastocyst grading) contains a description of 24 variables that are extracted from the image of the blastocyst and analyzed by three Artificial Neural Networks (ANNs) that classifies the same loaded image. The same embryo (i.e., the biological specimen) was submitted to digital image capture by the control group (inverted microscope with 40x of magnification) and to experimental group (stereomicroscope with maximum of magnification plus 4x zoom from the cell phone). The 36 images obtained from control and experimental groups were uploaded on the Blasto3Q. Each image from both sources was evaluated for segmentation and submitted (only if it could be properly or partially segmented) to the quality grade classification by the three ANNs of the Blasto3Q program. In the group control, all the images were properly segmented, whereas 38.9% (07/18) and 61.1% (11/18) of the images from the experimental group, respectively could not be segmented or were partially segmented. The percentage of agreement was calculated when the same blastocyst was evaluated by the same ANN from the two sources (control and experimental groups). On the 54 potential evaluations of the three ANNs (i.e., 18 images been evaluated by the three networks) from the experimental group only 22.2% agreed with evaluations of the control (12/54). Of the remaining 42 disagreed evaluations from experimental group, 21 were unable to be performed and 21 were wrongly processed when compared with control evaluation.

developmental biology↗

bioRxiv2022

Sfrp2 is a multifunctional regulator of rodent color patterns

Animal pigment patterns are excellent models to elucidate mechanisms of biological organization. Although theoretical simulations, such as Turing reaction-diffusion systems, recapitulate many animal patterns, they are insufficient to account for those showing a high degree of spatial organization and reproducibility. Here, we compare the coats of the African striped mouse (Rhabdomys pumilio) and the laboratory mouse (Mus musculus) to study the molecular mechanisms controlling stripe pattern formation. By combining transcriptomics, mathematical modeling, and mouse transgenics, we show that Sfrp2 regulates the distribution of hair follicles and establishes an embryonic prepattern that foreshadows pigment stripes. Moreover, by developing and employing in vivo gene editing experiments in striped mice, we find that Sfrp2 knockout is sufficient to alter the stripe pattern. Strikingly, mutants also exhibit changes in coat color, revealing an additional function of Sfrp2 in regulating hair color. Thus, a single factor controls coat pattern formation by acting both as an orienting signaling mechanism and a modulator of pigmentation. By uncovering a multifunctional regulator of stripe formation, our work provides insights into the mechanisms by which spatial patterns are established in developing embryos and the molecular basis of phenotypic novelty.

developmental biology↗

bioRxiv2023

Egr-2 coordinates intestinal remodeling by promoting midline patterning and pharynx regeneration in planarians

Regeneration requires remodeling of pre-existing structures and their integration with new cells and tissue. Identification of injury-induced regulators of these processes is central to regenerative biology. In planarian flatworms, the intestine remodels after amputation to re-establish normal morphology and integrate with the regenerating pharynx, the centrally located feeding organ. How these events are initiated and coordinated is currently unclear. In a candidate screen for injury-induced regulators of intestinal regeneration, we found that the transcription factor Early growth response protein 2 (Egr-2) was required for collective migration and fusion of intestinal branches at the anterior midline. Even though inhibition of egr-2 by RNA interference increased dorsoventral (DV) muscle fibers at the midline between intestinal branches, bulk RNA sequencing of regenerating tissue revealed negligible dysregulation of DV-, body wall-, or intestinal-muscle-associated transcripts. Instead, the midline polarity cue slit-1 and subsets of pharynx-associated transcripts were dysregulated. Both egr-2 and slit-1 RNAi delayed early pharynx regeneration, consistent with reduced slit-1 expression in egr-2(RNAi) regenerates in the region of pharynx specification. Furthermore, inhibition of pharynx regeneration regulators foxF-1 and foxA delayed integration with the intestine and disrupted formation of the intestines midline anterior branch. Our findings suggest that the pharynx plays an inductive role in initiation of intestinal remodeling, and demonstrate how injury-induced reprogramming influences subsequent tissue assembly and integration during regeneration.

developmental biology↗

bioRxiv2024

Eph/ephrin signalling in the developing brain is regulated by tissue stiffness

Eph receptors and their membrane-bound ligands, ephrins, provide key signals in many biological processes, such as cell proliferation, cell motility and cell sorting at tissue boundaries. However, despite immense progress in our understanding of Eph/ephrin signalling, there are still discrepancies between in vitro and in vivo work, and the regulation of Eph/ephrin signalling remains incompletely understood. Since a major difference between in vivo and most in vitro experiments is the stiffness of the cellular environment, we here investigated the interplay between tissue mechanics and Eph/ephrin signalling using the Xenopus laevis optic pathway as a model system. Xenopus retinal neurons cultured on soft substrates mechanically resembling brain tissue showed the opposite response to ephrinB1 compared to those cultured on glass. In vivo atomic force microscopy (AFM)-based stiffness mapping revealed that the visual area of the Xenopus brain, the optic tectum, becomes mechanically heterogeneous during its innervation by axons of retinal neurons. The resulting stiffness gradient correlated with both a cell density gradient and expression patterns of EphB and ephrinB family members. Exposing ex vivo brains to stiffer matrices or locally stiffening the optic tectum in vivo led to an increase in EphB2 expression in the optic tectum, indicating that tissue mechanics is an important regulator of Eph/ephrin signalling. Similar mechanisms are likely to be involved in the development and diseases of many other organ systems.

developmental biology↗

bioRxiv2025

A single-cell multiomics roadmap of zebrafish spermatogenesis reveals regulatory principles of male germline formation

Spermatogenesis is the biological process by which male sperm cells (spermatozoa) are produced in the testes. Beyond facilitating the transmission of genetic information, spermatogenesis also provides a potential framework for inter- and transgenerational inheritance of gene-regulatory states. While extensively studied in mammals, our understanding of spermatogenesis in anamniotes remains limited. Here we present a comprehensive single-cell multiomics resource, combining single-cell RNA sequencing (scRNA-seq) and single-cell chromatin accessibility (scATAC-seq) profiling, with base-resolution DNA methylome (WGBS) analysis of sorted germ cell populations from zebrafish (Danio rerio) testes. We identify major germ cell types involved in zebrafish spermatogenesis as well as key drivers associated with these transcriptional states. Moreover, we describe localised DNA methylation changes associated with spermatocyte populations, as well as local and global changes in chromatin accessibility leading to chromatin compaction in spermatids. Notably, we identify loci that evade global chromatin compaction, and which remain accessible, suggesting a potential mechanism for the intergenerational transmission of gene-regulatory states. Overall, this high-resolution atlas of zebrafish spermatogenesis provides a valuable resource for studying vertebrate germ cell development, evolution, and epigenetic inheritance.

developmental biology↗

bioRxiv2019

Amyloid precursor protein-b facilitates cell adhesion during early development in zebrafish

Understanding the biological function of amyloid beta (A{beta}) precursor protein (APP) beyond its role in Alzheimers disease is emerging. Yet, its function during embryonic development is poorly understood. The zebrafish APP homologue, Appb, is strongly expressed during early development but thus far has only been studied via morpholino-mediated knockdown. Zebrafish enables analysis of cellular processes in an ontogenic context, which is limited in many other vertebrates. We characterized zebrafish carrying a homozygous mutation that introduces a premature stop in exon 2 of the appb gene. We report that appb mutants are significantly smaller until 2dpf and display perturbed enveloping layer (EVL) integrity and cell protrusions at the blastula stage.\n\nMoreover, appb mutants surviving beyond 48 hpf exhibited no behavioral defects at 6 dpf and developed into healthy and fertile adults. The expression of the app-family members, appa and aplp2, was found to be altered in appb mutants. Taken together, we show that appb orchestrates the initial development by supporting the integrity of the EVL, likely by mediating cell adhesion properties. The loss of Appb might be compensated for by other app family members to be able to implement continued normal development.

developmental biology↗

bioRxiv2025

Repressive S-adenosylmethionine biosynthesis status inhibits transcription of HeT-A retrotransposon in the germline of Drosophila.

S-adenosylmethionine (SAM) is the principal cellular donor of methyl moiety in the methylation reaction and regulates gene expression by regulating methylation-related cellular events, such as epigenetic status. Although SAM biosynthesis affects a variety of biological phenomena including disease and aging, whether cell-specific SAM biosynthesis status is present and how it contributes to cellular function are largely unknown. Here, we firstly showed that the Drosophila germline in gametogenesis has a repressive SAM biosynthesis status through the observation of SAM synthetase (Sam-S), a key enzyme for SAM biosynthesis. In addition, our study showed that germline-unique repressive SAM biosynthesis status contributes to inhibition of retrotransposon expression; enhancement of SAM biosynthesis in germline caused excessive expression of retrotransposons including HeT-A, a telomere-specific retroelement, as the most affected target. We found that the promoter activity of HeT-A is enhanced in SAM increased condition with increased accumulation of 6mA DNA methylation, the major DNA methylation modification in the Drosophila genome. Interestingly, the enhanced 6mA enrichment and gene expression in enriched loci were not correlated in other retrotransposons or structural genes. Taken together, our results suggest that SAM-deficient status in the germline uniquely regulates HeT-A transcription via 6mA methylation modification. Thus, our study provides a new understanding of how germline unique metabolic status contributes to regulation of the retrotransposon.

developmental biology↗

bioRxiv2020

TAEL 2.0: An Improved Optogenetic Expression System for Zebrafish

Inducible gene expression systems are valuable tools for studying biological processes. We previously developed an optogenetic gene expression system called TAEL that is optimized for use in zebrafish. When illuminated with blue light, TAEL transcription factors dimerize and activate gene expression downstream of the TAEL-responsive C120 promoter. By using light as the inducing agent, the TAEL/C120 system overcomes limitations of traditional inducible expression systems by enabling fine spatial and temporal regulation of gene expression. Here, we describe ongoing efforts to improve the TAEL/C120 system. We made modifications to both the TAEL transcriptional activator and the C120 regulatory element, collectively referred to as TAEL 2.0. We demonstrate that TAEL 2.0 consistently induces higher levels of reporter gene expression and at a faster rate, but with comparable background and toxicity as the original TAEL system. With these improvements, we were able to create functional stable transgenic lines to express the TAEL 2.0 transcription factor either ubiquitously or with a tissue-specific promoter. We demonstrate that the ubiquitous line in particular can be used to induce expression at late embryonic and larval stages, addressing a major deficiency of the original TAEL system. This improved optogenetic expression system will be a broadly useful resource for the zebrafish community.

developmental biology↗

bioRxiv2021

ASC proneural transcription factors mediate the timely initiation of the neural program during neuroectodermal to neuroblast transition ensuring progeny fidelity

BackgroundASC/ASCL proneural transcription factors are oncogenic and exhibit impressive reprogramming and pioneer activities. In both Drosophila and mammals, these factors are central in the early specification of the neural fate, where they act in opposition to Notch signalling. However, the role of ASC on the chromatin during CNS neural stem cells birth remains elusive. ResultsWe investigated the chromatin changes accompanying neural commitment using an integrative genetics and genomics methodology. We found that ASC factors bind equally strongly to two distinct classes of cis-regulatory elements: open regions remodeled earlier during maternal to zygotic transition by Zelda and Zelda-independent, less accessible regions. Both classes cis-elements exhibit enhanced chromatin accessibility during neural specification and correlate with transcriptional regulation of genes involved in many biological processes necessary for neuroblast function. We identified an ASC-Notch regulated TF network that most likely act as the prime regulators of neuroblast function. Using a cohort of ASC target genes, we report that ASC null neuroblasts are defectively specified, remaining initially stalled, lacking expression of many proneural targets and unable to divide. When they eventually start proliferating, they produce compromised progeny. Generation of lacZ reporter lines driven by proneural-bound elements display enhancer activity within neuroblasts and proneural dependency. Therefore, the partial neuroblast identity seen in the absence of ASC genes is driven by other, proneural-independent, cis-elements. Neuroblast impairment and the late differentiation defects of ASC mutants are corrected by ectodermal induction of individual ASC genes but not by individual members of the TF network downstream of ASC. However, in wild type embryos induction of individual members of this network induces CNS hyperplasia, suggesting that they synergize with the activating function of ASC to establish the chromatin dynamics that promote neural specification. ConclusionASC factors bind a large number of enhancers to orchestrate the timely activation of the neural chromatin program during neuroectodermal to neuroblast transition. This early chromatin remodeling is crucial for both neuroblast homeostasis as well as future progeny fidelity.

developmental biology↗

bioRxiv2022

Single-Cell RNA-Seq Uncovers Dynamic Processes Orchestrated by RNA-Binding Protein DDX43 in Chromatin Remodeling during Spermiogenesis

Advances in single-cell RNA sequencing (scRNA-seq) have allowed for elucidating biological mechanisms at cell state level. Mammalian spermatogenic process showcases dynamic switches of gene expression pattern with delicate morphological and functional alterations of germ cells, but it is unclear how such dynamics is genetically controlled. Here we demonstrate that mouse testis-enriched RNA helicase DDX43, as well as its ATP hydrolysis site, is required for spermiogenesis. Genetic mutation of Ddx43 renders spermatids heterogeneously defective in multiple steps of chromatin remodeling, resulting in incomplete substitution of transition protein by protamine and less condensed sperm nucleus. Through scRNA-seq analyses of testicular cells derived from adult wild-type and Ddx43 mutant testes in mice, we reveal that the DDX43 deficiency-elicited perturbation in the dynamic RNA regulatory processes underlies the differentiation deficiency of spermatids. Further, focused analyses on early-stage spermatids combined with enhanced CLIP sequencing (eCLIP-seq) identify Elfn2 as DDX43-targeted hub gene, whose in vivo knockdown shows similar phenotypic defects as Ddx43 mutant. Our study illustrates an essential role for DDX43 in post-meiotic chromatin remodeling and highlights the single cell-based strategy for a refined dissection of stage-specific regulation of germline differentiation.

developmental biology↗

bioRxiv2023

A robust knock-in approach using a minimal promoter and a minicircle

Knock-in reporter (KI) animals are essential tools in biomedical research to study gene expression impacting diverse biological events. While CRISPR/Cas9-mediated genome editing allows for the successful generation of KI animals, several factors should be considered, such as low expression of the target gene, prevention of bacterial DNA integration, and in-frame editing. To circumvent these challenges, we developed a new strategy that utilizes minicircle technology and introduces a minimal promoter. We demonstrated that minicircles serve as an efficient donor DNA in zebrafish, significantly enhancing KI events compared to plasmids containing bacterial backbones. In an attempt to generate a KI reporter for scn8ab, we precisely integrated a fluorescence gene at the start codon. However, the seamlessly integrated reporter was unable to direct expression that recapitulates endogenous scn8ab expression. To overcome this obstacle, we introduced the hsp70 minimal promoter to provide an ectopic transcription initiation site and succeeded in establishing stable KI transgenic reporters for scn8ab. This strategy also created a fgf20b KI reporter line with a high success rate. Furthermore, our data revealed that an unexpectedly edited genome can inappropriately influence the integrated reporter gene expression, highlighting the importance of selecting a proper KI line. Overall, our approach utilizing a minicircle and an ectopic promoter establishes a robust and efficient strategy for KI generation, expanding our capacity to create KI animals.

developmental biology↗

bioRxiv2024

Tissue-specific and endogenous protein labeling with split fluorescent proteins

The ability to label proteins by fusion with genetically encoded fluorescent proteins is a powerful tool for understanding dynamic biological processes. However, current approaches for expressing fluorescent protein fusions possess drawbacks, especially at the whole organism level. Expression by transgenesis risks potential overexpression artifacts while fluorescent protein insertion at endogenous loci is technically difficult and, more importantly, does not allow for tissue-specific study of broadly expressed proteins. To overcome these limitations, we have adopted the split fluorescent protein system mNeonGreen21-10/11 (split-mNG2) to achieve tissue-specific and endogenous protein labeling in zebrafish. In our approach, mNG21-10 is expressed under a tissue-specific promoter using standard transgenesis while mNG211 is inserted into protein-coding genes of interest using CRISPR/Cas-directed gene editing. Each mNG2 fragment on its own is not fluorescent, but when co-expressed the fragments self-assemble into a fluorescent complex. Here, we report successful use of split-mNG2 to achieve differential labeling of the cytoskeleton genes tubb4b and krt8 in various tissues. We also demonstrate that by anchoring the mNG21-10 component to specific cellular compartments, the split-mNG2 system can be used to manipulate protein function. Our approach should be broadly useful for a wide range of applications.

developmental biology↗

bioRxiv2026

Holotomography reveals biophysical remodeling of mouse oocytes during post-ovulatory aging

Routine assessment of oocyte state in reproductive biology and clinical embryology still relies largely on two-dimensional transmitted-light morphology, leaving the underlying three-dimensional intracellular organization largely unmeasured. Here, we use holotomography to reconstruct volumetric refractive index (RI) distributions in unlabeled live mouse oocytes and combine this imaging with sparse-annotation, AI-assisted compartment segmentation and multidimensional feature extraction across geometry, RI statistics, dry-mass density, and intracellular texture. Applied to an in vitro model of post-ovulatory aging, holotomography-derived biophysical profiles separated fresh and aged oocytes more strongly than two-dimensional brightfield-derived features, and feature-family ablation indicated that non-morphological descriptors contributed substantially to this separation. At the population level, aged oocytes showed coordinated ooplasmic remodeling, including reduced volume, increased RI heterogeneity, and increased dry-mass density while total dry mass was broadly conserved. These findings demonstrate a label-free quantitative framework for detecting post-ovulatory aging-associated biophysical remodeling in intact mammalian oocytes. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=167 SRC="FIGDIR/small/733271v1_ufig1.gif" ALT="Figure 1"> View larger version (89K): org.highwire.dtl.DTLVardef@c7257aorg.highwire.dtl.DTLVardef@6d92f0org.highwire.dtl.DTLVardef@1c9f7eborg.highwire.dtl.DTLVardef@b36637_HPS_FORMAT_FIGEXP M_FIG C_FIG

Developmental Biology↗