Journal of Developmental Biology

14 pages, 4272 KB

Open AccessArticle

Cloned Pig Fetuses Have a High Placental Lysophosphatidylcholine Level That Inhibits Trophoblast Cell Activity

by Junkun Lai, Xiaoyu Gao, Guke Zhang, Xiao Wu, Yiqian Zhang, Shunbo Wang, Zhenfang Wu, Zicong Li and Zheng Xu

J. Dev. Biol. 2025, 13(4), 41; https://doi.org/10.3390/jdb13040041 - 12 Nov 2025

Abstract

Somatic cell nuclear transfer (SCNT) or cloning technology is widely used in agriculture and biomedicine. However, the application of this technology is limited by the low developmental competence of cloned embryos or fetuses, which frequently exhibit abnormal development of trophoblast cells or placentas. [...] Read more.

Somatic cell nuclear transfer (SCNT) or cloning technology is widely used in agriculture and biomedicine. However, the application of this technology is limited by the low developmental competence of cloned embryos or fetuses, which frequently exhibit abnormal development of trophoblast cells or placentas. The purpose of this study was to investigate the possible causes of the erroneous placental development of SCNT-derived pig fetuses. The placental transcriptomic and lipidomic profiles were compared between 30-day-old SCNT- and artificial insemination (AI)-produced pig fetuses. Differentially expressed lipid metabolites between two groups of placentas were selected to test their effects on porcine trophoblast cell activity. The results showed that SCNT placentas exhibit impaired lipid metabolism and function. The level of a metabolite, lysophosphatidylcholine (LPC), in the glycerophospholipid metabolism pathway was substantially increased in SCNT placentas, compared with AI placentas. The elevation in LPC content may lead to impaired placental development in cloned pig fetuses, as LPC inhibited the proliferation and migration of porcine trophoblast cells. This study discovers a main cause of erroneous development of cloned pig fetuses, which will be beneficial for understanding the regulation of SCNT embryo development, as well as developing new methods to improve the efficiency of pig cloning. Full article

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20 pages, 5140 KB

Open AccessReview

Defective Neural Stem and Progenitor Cell Proliferation in Neurodevelopmental Disorders

by Aki Shigenaka, Eri Nitta, Tadashi Nakagawa, Makiko Nakagawa and Toru Hosoi

J. Dev. Biol. 2025, 13(4), 40; https://doi.org/10.3390/jdb13040040 - 7 Nov 2025

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Abstract

Neurodevelopmental disorders (NDDs), including autism spectrum disorder, intellectual disability, and attention deficit hyperactivity disorder, are increasingly recognized as disorders of early brain construction arising from defects in neural stem and progenitor cell (NSPC) proliferation. NSPCs are responsible for generating the diverse neuronal and [...] Read more.

Neurodevelopmental disorders (NDDs), including autism spectrum disorder, intellectual disability, and attention deficit hyperactivity disorder, are increasingly recognized as disorders of early brain construction arising from defects in neural stem and progenitor cell (NSPC) proliferation. NSPCs are responsible for generating the diverse neuronal and glial lineages that establish cortical architecture and neural circuitry; thus, their expansion must be tightly coordinated by intrinsic cell cycle regulators and extrinsic niche-derived cues. Disruption of these mechanisms—through genetic mutations, epigenetic dysregulation, or environmental insults—can perturb the balance between NSPC self-renewal and differentiation, resulting in aberrant brain size and connectivity. Recent advances using animal models and human pluripotent stem cell-derived brain organoids have identified key signaling pathways, including Notch, Wnt, SHH, and PI3K–mTOR, as central hubs integrating proliferative cues, while transcriptional and chromatin regulators such as PAX6, CHD8, SETD5, and ANKRD11 govern gene expression essential for proper NSPC cycling. Furthermore, prenatal exposure to teratogens such as Zika virus infection, valproic acid, or metabolic stress in phenylketonuria can recapitulate proliferation defects and microcephaly, underscoring the vulnerability of NSPCs to environmental perturbation. This review summarizes emerging insights into the molecular and cellular mechanisms by which defective NSPC proliferation contributes to NDD pathogenesis, highlighting convergence among genetic and environmental factors on cell cycle control. A deeper understanding of these pathways may uncover shared therapeutic targets to restore neurodevelopmental trajectories and mitigate disease burden. Full article

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19 pages, 2414 KB

Open AccessReview

Recapitulating Liver Embryology—Lessons to Be Learned for Liver Diseases

by Rui Caetano Oliveira, Sandra Ferreira, Isabel Gonçalves and Maria Fátima Martins

J. Dev. Biol. 2025, 13(4), 39; https://doi.org/10.3390/jdb13040039 - 4 Nov 2025

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Abstract

Despite looking monotonous, liver histology represents a highly complex structure of hepatocytes, bile ducts and vessels. This complex interaction and development originate in embryology and remain in adult life. In this manuscript, we highlight the features of liver embryology, translating the events into [...] Read more.

Despite looking monotonous, liver histology represents a highly complex structure of hepatocytes, bile ducts and vessels. This complex interaction and development originate in embryology and remain in adult life. In this manuscript, we highlight the features of liver embryology, translating the events into pathologic features and opening possibilities for disease understanding and research. We revisit liver embryology, from biliary to vascular processes, stressing some developing abnormalities with a focus on the histological findings. With this manuscript, we hope to increase the awareness of the importance of embryology in diseases, prompting its detailed study. Full article

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19 pages, 1862 KB

Open AccessArticle

Activity-Dependent Increases in Quantal Size at the Drosophila NMJ

by Andrew S. Powers, Petar Gajic, Ethan Rittereiser, Kavindra Dasrat and Gregory A. Lnenicka

J. Dev. Biol. 2025, 13(4), 38; https://doi.org/10.3390/jdb13040038 - 28 Oct 2025

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Abstract

We examined whether an increase in synaptic activity resulted in an increase in quantal size at the neuromuscular junction (NMJ) of third-instar Drosophila larvae. Spontaneous miniature excitatory postsynaptic currents (mEPSCs) or miniature excitatory postsynaptic potentials (mEPSPs) were recorded before and after nerve stimulation. [...] Read more.

We examined whether an increase in synaptic activity resulted in an increase in quantal size at the neuromuscular junction (NMJ) of third-instar Drosophila larvae. Spontaneous miniature excitatory postsynaptic currents (mEPSCs) or miniature excitatory postsynaptic potentials (mEPSPs) were recorded before and after nerve stimulation. We found that prolonged (60 s) or brief (1.25 s) nerve stimulation produced an increase in quantal size; this appears to be a general property of these synapses since it was seen at all four muscle fibers (MFs) used in this study. The effect was examined along Is and Ib terminals by expressing GCaMP in the MF membrane and examining postsynaptic Ca²⁺ signals produced by spontaneous transmitter release. The activity-dependent increase in quantal size occurred at both Is and Ib terminals, and the increase in frequency and amplitude of quantal events at individual synaptic boutons was correlated. Both the increase in quantal size and frequency were found to be dependent upon an increase in postsynaptic Ca²⁺, based on studies in which MFs were preinjected with the Ca²⁺ chelator BAPTA (1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid). To examine the effect of postsynaptic activity on glutamate sensitivity, we iontophoresed glutamate pulses at the NMJ and recorded the glutamate-evoked excitatory postsynaptic potentials (gEPSPs). Trains of glutamate pulses produced an increase in gEPSP amplitude; this potentiation was not seen when Ca²⁺ was eliminated from the bath or after inhibiting calmodulin or CaMKII. The activity-dependent increase in quantal size may result from an increase in postsynaptic sensitivity due to activation of CaMKII. Full article

(This article belongs to the Special Issue Drosophila in Developmental Biology—Past, Present and Future)

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18 pages, 1576 KB

Open AccessArticle

A Supra-Physiological Dose of 2-Hydroxyestradiol Impairs Meiotic Progression and Developmental Competence of Mouse Antral Oocytes

by Valeria Merico, Paola Rebuzzini, Mario Zanoni, Maurizio Zuccotti and Silvia Garagna

J. Dev. Biol. 2025, 13(4), 37; https://doi.org/10.3390/jdb13040037 - 15 Oct 2025

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Abstract

Estrogen metabolites (EMs) play a local regulatory role in mammalian ovarian function. Among them, 2-hydroxyestradiol (2-OHE2) exerts dose-dependent effects on reproductive physiology, supporting either normal ovarian processes or contributing to pathological conditions. Specifically, 2-OHE2 modulates ovarian vasculature and progesterone biosynthesis, and at 1–10 [...] Read more.

Estrogen metabolites (EMs) play a local regulatory role in mammalian ovarian function. Among them, 2-hydroxyestradiol (2-OHE2) exerts dose-dependent effects on reproductive physiology, supporting either normal ovarian processes or contributing to pathological conditions. Specifically, 2-OHE2 modulates ovarian vasculature and progesterone biosynthesis, and at 1–10 nM concentrations, it enhances in vitro developmental competence and blastocyst quality in mouse oocytes. Conversely, doses below 1 nM show no appreciable effects, suggesting the existence of a biological activity threshold. However, the impact of supra-physiological concentrations remains largely unexplored. In this study, we investigated the effects of increasing 2-OHE2 doses (0.05, 0.50, and 5.00 µM) on oocyte meiotic progression and quality. Exposure to 0.50 and 5.00 µM significantly impaired oocyte maturation, while only the highest dose notably reduced the percentage of embryos developing to the blastocyst stage. Morphometric analysis during the GV-to-MII transition revealed altered first polar body morphology, defective asymmetric division, and disruptions in cytoskeletal organization, including enlarged meiotic spindles, increased F-actin cap angles, and aberrant microtubule-organizing centers distribution. These structural alterations were paralleled by distinct changes in cytoplasmic movement velocity patterns observed through time-lapse imaging during meiotic resumption. Together, these findings demonstrate that supra-physiological exposure to 2-OHE2 compromises oocyte maturation and developmental competence by perturbing key cytoskeletal dynamics and cellular architecture necessary for successful meiosis and early embryogenesis. Full article

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24 pages, 3343 KB

Open AccessReview

An Integrated Canonical and Non-Canonical Wnt Signaling Network Controls Early Anterior–Posterior Axis Formation in Sea Urchin Embryos

by Jennifer L. Fenner, Boyuan Wang, Cheikhouna Ka, Sujan Gautam and Ryan C. Range

J. Dev. Biol. 2025, 13(4), 36; https://doi.org/10.3390/jdb13040036 - 8 Oct 2025

Viewed by 673

Abstract

Wnt signaling is an ancient developmental mechanism that drives the initial specification and patterning of the primary axis in many metazoan embryos. Yet, it is unclear how exactly the various Wnt components interact in most Wnt-mediated developmental processes as well as in the [...] Read more.

Wnt signaling is an ancient developmental mechanism that drives the initial specification and patterning of the primary axis in many metazoan embryos. Yet, it is unclear how exactly the various Wnt components interact in most Wnt-mediated developmental processes as well as in the molecular mechanism regulating adult tissue homeostasis. Recent work in invertebrate deuterostome sea urchin embryos indicates that three different Wnt signaling pathways (Wnt/β-catenin, Wnt/JNK, and Wnt/PKC) form an interconnected Wnt signaling network that specifies and patterns the primary anterior–posterior (AP) axis. Here, we detail our current knowledge of this critical regulatory process in sea urchin embryos. We also illustrate examples from a diverse group of metazoans, from cnidarians to vertebrates, that suggest aspects of the sea urchin AP Wnt signaling network are deeply conserved. We explore how the sea urchin is an excellent model to elucidate a detailed molecular understanding of AP axis specification and patterning that can be used for identifying unifying developmental principles across animals. Full article

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26 pages, 2513 KB

Open AccessArticle

High Concentrations of Non-Esterified Fatty Acids During Bovine In Vitro Fertilisation Are Detrimental for Spermatozoa Quality and Pre-Implantation Embryo Development

by Abdullah F. Idriss, Edward J. Okello, Roger G. Sturmey and Miguel A. Velazquez

J. Dev. Biol. 2025, 13(4), 35; https://doi.org/10.3390/jdb13040035 - 5 Oct 2025

Viewed by 970

Abstract

High non-esterified fatty acids (NEFAs) during negative energy balance in dairy cattle can impair reproduction. While their effects on oocyte maturation and preimplantation embryo development are known, their impact during fertilisation is largely unexplored. This study examined the effects of high NEFA exposure [...] Read more.

High non-esterified fatty acids (NEFAs) during negative energy balance in dairy cattle can impair reproduction. While their effects on oocyte maturation and preimplantation embryo development are known, their impact during fertilisation is largely unexplored. This study examined the effects of high NEFA exposure exclusively during in vitro fertilisation (IVF). Bovine oocytes were matured in vitro and fertilised under physiological or high NEFA concentrations. High NEFA concentrations decreased fertilisation, cleavage, and blastocyst rates. Reactive oxygen species production in zygotes was not affected, but blastocysts derived from the High-NEFA group had fewer cells. Spermatozoa exposed to high NEFA concentrations exhibited increased plasma membrane and acrosome damage, higher DNA fragmentation, and reduced mitochondrial membrane potential. The expression of H3K27me3, a repressive histone mark normally erased from fertilisation to embryonic genome activation, was higher in 2-cell than in 4-cell embryos on day 2 after IVF, but only in the High-NEFA group. This delayed H3K27me3 loss, along with increased DNA damage, could partially explain the reduced blastocyst formation observed. In conclusion, high NEFA concentrations can impair pre-implantation embryo development during zygote formation, potentially via effects on both the oocyte and spermatozoon. The latter warrants further investigation using an intracytoplasmic sperm injection model. Full article

(This article belongs to the Special Issue Embryonic Development and Regenerative Medicine)

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14 pages, 1861 KB

Open AccessBrief Report

Exploring the Regulation of Tmem182 Gene Expression in the Context of Retinoid X Receptor Signaling

by Saadia Khilji, Munerah Hamed, Jihong Chen and Qiao Li

J. Dev. Biol. 2025, 13(4), 34; https://doi.org/10.3390/jdb13040034 - 24 Sep 2025

Viewed by 480

Abstract

We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor (RXR), promotes the differentiation and fusion of skeletal myoblasts. We have also analyzed the genomic programs underlying rexinoid-enhanced myogenic differentiation to identify novel regulatory pathways. As such, we observed [...] Read more.

We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor (RXR), promotes the differentiation and fusion of skeletal myoblasts. We have also analyzed the genomic programs underlying rexinoid-enhanced myogenic differentiation to identify novel regulatory pathways. As such, we observed a significant upregulation of a transcript encoding a predicted transmembrane protein, Tmem182, during C2C12 myoblast differentiation. Despite the documentation of Tmem182 expression in skeletal muscles, its regulation had yet to be explored. Here, we show that Tmem182 gene expression is markedly augmented in early myoblast differentiation and further enhanced by RXR signaling. In addition, Tmem182 expression is specific to muscle tissues and related to muscle master regulator MyoD. We found that MyoD and histone acetyltransferase p300 are bound to the Tmem182 promoter, and Tmem182 expression is p300-dependent. Thus, our data display a putative epigenetic signature associated with p300 and histone acetylation in rexinoid-responsive locus activation and transcription of myogenic targets. Full article

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J. Dev. Biol., Volume 13, Issue 4 (December 2025) – 8 articles

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