Ectodermal Layer Research Articles

Periderm fate and independence of tooth formation are conserved across osteichthyans

BackgroundPrevious studies have reported that periderm (the outer ectodermal layer) in zebrafish partially expands into the mouth and pharyngeal pouches, but does not reach the medial endoderm, where the pharyngeal teeth develop. Instead, periderm-like cells, arising independently from the outer periderm, cover prospective tooth-forming epithelia and are crucial for tooth germ initiation. Here we test the hypothesis that restricted expansion of periderm is a teleost-specific character possibly related to the derived way of early embryonic development. To this end, we performed lineage tracing of the periderm in a non-teleost actinopterygian species possessing pharyngeal teeth, the sterlet sturgeon (Acipenser ruthenus), and a sarcopterygian species lacking pharyngeal teeth, the axolotl (Ambystoma mexicanum).ResultsIn sturgeon, a stratified ectoderm is firmly established at the end of gastrulation, with minimally a basal ectodermal layer and a surface layer that can be homologized to a periderm. Periderm expands to a limited extent into the mouth and remains restricted to the distal parts of the pouches. It does not reach the medial pharyngeal endoderm, where pharyngeal teeth are located. Thus, periderm in sturgeon covers prospective odontogenic epithelium in the jaw region (oral teeth) but not in the pharyngeal region. In axolotl, like in sturgeon, periderm expansion in the oropharynx is restricted to the distal parts of the opening pouches. Oral teeth in axolotl develop long before mouth opening and possible expansion of the periderm into the mouth cavity.ConclusionsRestricted periderm expansion into the oropharynx appears to be an ancestral feature for osteichthyans, as it is found in sturgeon, zebrafish and axolotl. Periderm behavior does not correlate with presence or absence of oral or pharyngeal teeth, whose induction may depend on ‘ectodermalized’ endoderm. It is proposed that periderm assists in lumenization of the pouches to create an open gill slit. Comparison of basal and advanced actinopterygians with sarcopterygians (axolotl) shows that different trajectories of embryonic development converge on similar dynamics of the periderm: a restricted expansion into the mouth and prospective gill slits.

Detection of an EDA mutation causing hypohidrotic ectodermal dysplasia in a Vietnamese patient

Hypohidrotic ectodermal dysplasia (HED) is a rare disease characterized by abnormal development of the structures derived from the ectoderm layer, including hair, teeth, nails, and sweat glands. The most observed form of HED, which is known as X-linked hypohidrotic ectodermal dysplasia (XLHED), is commonly attributed to genetic abnormalities in the ectodysplasin A (EDA) gene. We have successfully discovered a known mutation c.1045G>A (p.A349T) in a Vietnamese proband who displayed the main symptoms of XLHED using PCR and Sanger sequencing. Furthermore, the segregation of the mutation showed that the mother, who exhibited a normal phenotype, was a carrier of the mutation, while the father was hemizygous for the wild-type allele. The identification of the mutation c.1045G>A (p.A349T) contributes to HED research worldwide and can be used for genetic counseling in Vietnam.

Tracking cell layer contribution during repair of the tympanic membrane.

The tympanic membrane (i.e. eardrum) sits at the interface between the middle and external ear. The tympanic membrane is composed of three layers: an outer ectoderm-derived layer, a middle neural crest-derived fibroblast layer with contribution from the mesoderm-derived vasculature, and an inner endoderm-derived mucosal layer. These layers form a thin sandwich that is often perforated following trauma, pressure changes or middle ear inflammation. During healing, cells need to bridge the perforation in the absence of an initial scaffold. Here, we assessed the contribution, timing and interaction of the different layers during membrane repair by using markers and reporter mice. We showed that the ectodermal layer is retracted after perforation, before proliferating away from the wound edge, with keratin 5 basal cells migrating over the hole to bridge the gap. The mesenchymal and mucosal layers then used this scaffold to complete the repair, followed by advancement of the vasculature. Finally, differentiation of the epithelium led to formation of a scab. Our results reveal the dynamics and interconnections between the embryonic germ layers during repair and highlight how defects might occur.

Gastrulation: Its Principles and Variations.

As epiblast cells initiate development into various somatic cells, they undergo a large-scale reorganization, called gastrulation. The gastrulation of the epiblast cells produces three groups of cells: the endoderm layer, the collection of miscellaneous mesodermal tissues, and the ectodermal layer, which includes the neural, epidermal, and associated tissues. Most studies of gastrulation have focused on the formation of the tissues that provide theprimary route for cell reorganization, that is, the primitive streak, in the chicken and mouse. In contrast, how gastrulation alters epiblast-derived cells has remained underinvestigated. This chapter highlights the regulation of cell and tissue fate via the gastrulation process. The roles and regulatory functions of neuromesodermal progenitors (NMPs) in the gastrulation process, elucidated in the last decade, are discussed in depth to resolve points of confusion. Chicken and mouse embryos, which form a primitive streak as the site of mesoderm precursor ingression, have been investigated extensively. However, primitive streak formation is an exception, even among amniotes. The roles of gastrulation processes in generating various somatic tissues will be discussed broadly.

Caspase-mediated LPS sensing and pyroptosis signaling in Hydra.

Inflammatory caspases sensing lipopolysaccharide (LPS) to drive gasdermin (GSDM)-mediated pyroptosis is an important immune response mechanism for anti-infection defense in mammals. In this work, we resolved an LPS-induced and GSDM-gated pyroptosis signaling cascade in Cnidarians. Initially, we identified a functional GSDM protein, HyGSDME, in Hydra, executing cytosolic LPS-induced pyroptosis in a caspase-dependent manner. Further, we identified a proinflammatory caspase, HyCaspA, capable of sensing cytosolic LPS by an uncharacterized N-terminal domain relying on its unique hydrophobic property, thereby triggering its oligomerization and self-activation. Subsequently, the LPS-activated HyCaspA cleaved an apoptotic caspase, HyCARD2, to trigger HyGSDME-gated pyroptosis. Last, HyGSDME exhibited an enriched distribution on the ectodermal layer of Hydra polyps, exerting a canonical immune defense function against surface-invading bacteria. Collectively, our work resolved an ancient pyroptosis signaling cascade in Hydra, suggesting that inflammatory caspases sensing cytosolic LPS to initiate GSDM-gated pyroptosis are a conserved immune defense mechanism from Cnidarians to mammals.

The surface ectoderm exhibits spatially heterogenous tension that correlates with YAP localisation during spinal neural tube closure in mouse embryos

The single cell layer of surface ectoderm (SE) which overlies the closing neural tube (NT) plays a crucial biomechanical role during mammalian NT closure (NTC), challenging previous assumptions that it is only passive to the force-generating neuroepithelium (NE). Failure of NTC leads to congenital malformations known as NT defects (NTDs), including spina bifida (SB) and anencephaly in the spine and brain respectively. In several mouse NTD models, SB is caused by misexpression of SE-specific genes and is associated with disrupted SE mechanics, including loss of rostrocaudal cell elongation believed to be important for successful closure. In this study, we asked how SE mechanics affect NT morphology, and whether the characteristic rostrocaudal cell elongation at the progressing closure site is a response to tension anisotropy in the SE. We show that blocking SE-specific E-cadherin in ex utero mouse embryo culture influences NT morphology, as well as the F-actin cable. Cell border ablation shows that cell shape is not due to tension anisotropy, but that there are regional differences in SE tension. We also find that YAP nuclear translocation reflects regional tension heterogeneity, and that its expression is sensitive to pharmacological reduction of tension. In conclusion, our results confirm that the SE is a biomechanically important tissue for spinal NT morphogenesis and suggest a possible role of spatial regulation of cellular tension which could regulate downstream gene expression via mechanically-sensitive YAP activity.

Ectodysplasin A1 Deficiency Leads to Osteopetrosis-like Changes in Bones of the Skull Associated with Diminished Osteoclastic Activity.

Pathogenic variants of the gene Eda cause X-linked hypohidrotic ectodermal dysplasia (XLHED), which is characterized by structural abnormalities or lack of ectodermal appendages. Signs of dysplasia are not restricted to derivatives of the ectodermal layer, but mesodermal abnormalities, such as craniofacial dysmorphism, are also frequently observed, suggesting close reciprocal interactions between the ectoderm and mesoderm; however, a causal link has remained unsubstantiated. We investigated the functional impact of defective ectodysplasin A1 (Eda1) signaling on postnatal bone homeostasis in Eda1-deficient Tabby mice. Interestingly, Eda1 was detected in wild-type mouse calvariae throughout postnatal lifetime. In calvariae, bone-lining Osterix (Osx)+ osteoblasts stained positive for Eda1, and osteoclasts were revealed as Eda receptor (Edar)-positive. Moreover, adult Eda1-deficient calvarial bone showed osteopetrosis-like changes with significantly diminished marrow space, which was maintained during adulthood. Concomitantly with osteopetrosis-like changes, Tabby calvarial bone and Tabby bone marrow-derived osteoclasts had far less osteoclastic activity-associated co-enzymes including cathepsin K, Mmp9, Trap, and Tcirg1 (V-type proton ATPase a3 subunit) compared with wild-type calvariae in vivo or osteoclasts in vitro, indicating that Eda1 deficiency may affect the activity of osteoclasts. Finally, we confirmed that nuclear Nfatc1-positive osteoclasts were strongly diminished during mature osteoclastic differentiation under M-CSF and RANKL in the Tabby model, while Fc-EDA treatment of Tabby-derived osteoclasts significantly increased nuclear translocation of Nfatc1. Furthermore, we identified enhanced Nfatc1 and NF-κB transcriptional activity following Fc-EDA treatment in vitro using luciferase assays. Overall, the results indicate that diminished expressions of osteoclastic activity-associated co-enzymes may lead to disturbed bone homeostasis in Tabby calvariae postnatally.

Proximal ventricular shunt catheter occlusion model.

Proximal ventricular shunt catheter occlusion remains a problematic cause of shunt malfunction, and there is no consistent in vivo or in vitro model to help clinicians and researchers study this phenomenon. An in vitro model utilizing standard proximal ventricular catheter and biological occluding agents mimicking choroid plexus was designed, constructed, and calibrated to occlude consistently within a specified timeframe. Hydrostatic pressure differential of 100 cmH2O was used as a driving force to generate flow through the catheter. Chalaza and vitelline membranes were harvested from avian eggs and used as occluding agents. Successful occlusion was defined as a greater than 90% reduction in volumetric flow rate through distal outlet. Histological sections of occluded catheters were performed and interpreted by a neuropathologist. Initial trials demonstrated successful standard catheter occlusion within 24h using chalaza, vitelline membrane, and combination treatments. Repeat trials demonstrated consistency in successful occlusion within 5min utilizing only vitelline membrane treatment. Histopathology demonstrated the vitelline membrane to consist of a thin, superficial layer of extraembryonic ectoderm; the chalaza was observed to consist of strands of mucin protein. An in vitro model of proximal ventricular shunt catheter occlusion was developed and calibrated for successful occlusion within 5min. Future studies may utilize this model to rapidly test occlusion-resistant shunt designs and de-obstruction techniques.

Abstract 2634: Vasoactive intestinal polypeptide (VIP) regulates ZEB1 expression in cancer

Abstract Background: In cancer immunology, VIP is a neuropeptide with pleiotropic effects that include inhibiting T cell activation, increasing Treg frequency, and augmenting the myeloid-derived suppressor cells function. VIP expression by cancer may represent a paracrine immune-checkpoint pathway while simultaneously having autocrine effects on cancer growth. We used an in silico model to identify genes whose over-expression in cancer was correlated with VIP expression and confirmed the role of VIP receptor (VIPR) signaling in vitro using VIPR inhibitors. Methods: The TCGA PanCan dataset (UCSC Xena) was used to compare mRNA expression data of VIP versus 760 genes involved in 48 cancer related pathways. Associations by cancer histology and germ layer were calculated. A Pearson’s Coefficient cutoff of R > [0.3] defined a significant gene association. VIP and target gene expression were confirmed and quantified by western blot analysis in cancer cell lines and VIPR signaling was inhibited using ANT008, a novel VIPR inhibitor. Results: Significant associations were observed between VIP expression and 10 genes (Table 1). Strong associations (R > [0.4]) were observed in cancers derived from ectodermal and mesodermal germ layers. The strongest gene association was for VIP and ZEB1 in stomach adenocarcinoma (STAD, R = 0.7643). In vitro experiments using Jurkat T cells confirmed expression of VIP and ZEB1 proteins. Treatment with the VIPR inhibitor ANT008 (10μM) reduced VIP and ZEB1 protein expression by 50%. A similar fold increase in ZEB1 expression was observed with exogenous VIP. PCR studies are currently underway. Conclusions: The results demonstrate autocrine signaling between VIP expression and cancer associated gene pathways. ZEB1 is a known EMT (epithelial mesenchymal transition) regulator, and our in vitro studies novelly link VIP to EMT and demonstrate that this pathway is therapeutically targetable using a VIPR inhibitor. Further studies in the pertinent tumor histologies are warranted. Table 1. Genes All Samples Ectoderm (All) Mesoderm (All) Endoderm (All) MAPK3 0.3120 0.3537 0.2252 0.3380 ZEB1 0.3621 0.4341 0.4901 0.3348 NOS2 0.3611 0.3186 0.4849 0.3428 TEK 0.3113 0.3336 0.5131 0.2600 PTCH1 0.3031 0.4040 -0.0061 0.2879 EI4G1 -0.3216 -0.4268 -0.3779 -0.2064 GMPS -0.3074 -0.4698 -0.3005 -0.0928 CDK2 -0.3186 -0.4687 -0.2345 -0.0563 RUVBL1 -0.3135 -0.3270 -0.4716 -0.1886 TIMELESS -0.3036 -0.4284 -0.3717 -0.1505 Citation Format: Ishani H. Rao, Rohan Dhamsania, Edmund K. Waller, Sanjay Chandrasekaran. Vasoactive intestinal polypeptide (VIP) regulates ZEB1 expression in cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2634.

YAP1 regulates the self-organized fate patterning of hESC-derived gastruloids.

SummaryThe gastrulation process relies on complex interactions between developmental signaling pathways that are not completely understood. Here, we interrogated the contribution of the Hippo signaling effector YAP1 to the formation of the three germ layers by analyzing human embryonic stem cell (hESC)-derived 2D-micropatterned gastruloids. YAP1 knockout gastruloids display a reduced ectoderm layer and enlarged mesoderm and endoderm layers compared with wild type. Furthermore, our epigenome and transcriptome analysis revealed that YAP1 attenuates Nodal signaling by directly repressing the chromatin accessibility and transcription of key genes in the Nodal pathway, including the NODAL and FOXH1 genes. Hence, in the absence of YAP1, hyperactive Nodal signaling retains SMAD2/3 in the nuclei, impeding ectoderm differentiation of hESCs. Thus, our work revealed that YAP1 is a master regulator of Nodal signaling, essential for instructing germ layer fate patterning in human gastruloids.

Ectodermal Dysplasia: A Case Report

Ectodermal dysplasia (ED) is a hereditary genetic disorder that manifests a variety of deformities in one or more of the ectodermal derivatives. Ectodermal derivatives originate from ectodermal layers during embryonic development, such as skin, nails, hair, teeth, and exocrine glands. Over 150 variants of ED are reported in the literature. It has an incidence of seven in every 100,000 live births. There are two types of ED, which are hypohidrotic (anhidrotic) and hydrotic. The types are classified according to the degree of function of the sweat glands. This report discusses the case of a 13-month-old Saudi girl with typical features of ectodermal dysplasia who presented to a dermatology clinic.

Clinical experience of observation and tactics of management of a patient with ectodermal angydrotic dysplasia

The concept of ectodermal dysplasias covers a group of rare hereditary developmental anomalies that have a variety of phenotypic variants, but are characterized by common signs of underdevelopment or abnormal formation of organs and tissues derived from the ectodermal layer (skin and its derivatives - nails, hair, teeth, nervous system and sensory organs) ... Approximately 25% of ectodermal dysplasias known to date are inherited in an autosomal dominant or autosomal recessive manner; in other cases, the mode of inheritance is unclear. The syndrome is characterized by a wide range of clinical manifestations and may include additional symptoms of damage to other ectodermal, mesodermal, and endodermal structures. Ectodermal anomalies are a manifestation of disturbances in spatial-temporal coordination during the development of the epidermis. They involve genes such as EGF (epidermal growth factor), ED1 (ectodisplasin), EDAR (anhydrotic receptor ectodysplasin 1) and others that regulate the activity of genes involved in epidermal morphogenesis by activating or suppressing transcription factors (in particular, pb3; Koster). So far, only about 20% of genes have been identified that are responsible for about 200 ectodermal dysplasias of various symptoms and severity. This article describes the clinical observation of a patient with a rare disease - ectodermal anhydrotic dysplasia. The literature data on the clinical features of the course of this dermatosis, as well as the features of the course in this patient are presented.

Molecular basis of ectodermal dysplasia

Ectodermal dysplasia (ED) syndrome is a rare genetic disease that involves a heterogeneous group of hereditary disorders that occur as a result of mutations in genes that code for development of fetal ectoderm and lead to numerous disorders. Defects in the development of the ectoderm cause symptoms in tissues derived from the ectoderm layer, such as skin, nails, hair, and teeth. Because many pathways are involved in the development of the ectoderm, there are mutations in many genes that cause ED. Owing to the heterogeneity of ED, there are different types of the disease that have different symptoms. These symptoms include sparse hair, abnormal or missing teeth, nail dystrophy, lack of sweating owing to the absence of sweat glands, and cancer. In this review, in addition to discussing the role and pathway of each of the genes involved in ED, the incidence of cancer in these patients, diagnostic methods and differentiation from other similar diseases, and the treatments currently being performed for ED are discussed.

A p53-dependent translational program directs tissue-selective phenotypes in a model of ribosomopathies.

In ribosomopathies, perturbed expression of ribosome components leads to tissue-specific phenotypes. What accounts for such tissue-selective manifestations as a result of mutations in the ribosome, a ubiquitous cellular machine, has remained a mystery. Combining mouse genetics and invivo ribosome profiling, we observe limb-patterning phenotypes in ribosomal protein (RP) haploinsufficient embryos, and we uncover selective translational changes of transcripts that controlling limb development. Surprisingly, both loss of p53, which is activated by RP haploinsufficiency, and augmented protein synthesis rescue these phenotypes. These findings are explained by the finding that p53 functions as a master regulator of protein synthesis, at least in part, through transcriptional activation of 4E-BP1. 4E-BP1, a key translational regulator, in turn, facilitates selective changes in the translatome downstream of p53, and this thereby explains how RP haploinsufficiency may elicit specificity to gene expression. These results provide an integrative model to help understand how invivo tissue-specific phenotypes emerge in ribosomopathies.

Atypical Presentation of Complicated Dermoid Cyst of Ovary Mimicking Diverticular Abscess

Background: Cystic teratomas comprises 20% overall among all ovarian neoplasia. They are made of derivatives of at least two of three germ layers. Histologically different dermoid cyst contains only well differentiated embryological elements of ectodermal layer. Diverticulitis of colon mainly affects elderly population having abscess formation causing lower abdominal pain. Case presentation: We report a case of 50 yr old woman presenting with lower abdominal pain. From barium enema, ultrasound and CT we suggested the probability of diverticular abscess. Patient was undergone left salpingo-oophorectomy with repair of adhered part of sigmoid colon. Post op biopsy shows typical features of dermoid cyst. Conclusions: We illustrate how a dermoid cyst may be diagnosed as diverticular abscess by imaging. We also showed the rupture of dermoid cyst into sigmoid colon with communication formation. So we the radiologists must be aware of all possible differential diagnosis of lower abdominal pain in elderly female, so that we can help our fellow surgeons to treat properly. Keywords: Cystic teratoma, Diverticulitis, Post menopausal, Sigmoid Colon.

Anhidrotic ectodermal dysplasia in infancy – Case of misconduct of hyperthermia

Ectodermal dysplasias are a group of hereditary disorders with improper development of embryonal ectodermal layer. The diagnosis of these disorders is challenging during infancy and it must be considered while investigating infants or neonates with fever without focus and dehydration. In the infants, clinical signs of this condition are subtle and non-specific. The classical signs of the disease become more visible after a few months of life. Paediatricians should have high index of suspicion of anhidrotic ectodermal dysplasia in infants or neonates presenting with fever without focus and dehydration especially in summer season. We report this rare clinical entity and supplicate to consider the diagnosis of anhidrotic ectodermal dysplasia when investigating pyrexia of unknown origin (PUO) or hyperthermia in infants during summer especially in areas of semi arid climate and dry weather. Keywords: External dysplasia, Anhidrotic, Pyrexia of unknown origin.

Repression of Inappropriate Gene Expression in the Vertebrate Embryonic Ectoderm.

During vertebrate embryogenesis, precise regulation of gene expression is crucial for proper cell fate determination. Much of what we know about vertebrate development has been gleaned from experiments performed on embryos of the amphibian Xenopus laevis; this review will focus primarily on studies of this model organism. An early critical step during vertebrate development is the formation of the three primary germ layers—ectoderm, mesoderm, and endoderm—which emerge during the process of gastrulation. While much attention has been focused on the induction of mesoderm and endoderm, it has become clear that differentiation of the ectoderm involves more than the simple absence of inductive cues; rather, it additionally requires the inhibition of mesendoderm-promoting genes. This review aims to summarize our current understanding of the various inhibitors of inappropriate gene expression in the presumptive ectoderm.

The levels of fetuin-a, osteopontin, total antioxidant and oxidant in patients with midline closure defects

Amaç: Orta Hat kapanma Defekti (OHD) yüksek morbidite ve mortalite ile ilişkili doğumsal spinal omurgaların birleşme kusurudur. OHD’li olan hastalarda Fetuin-A, Osteopontin, Total antioksidan ve oksidan seviyeleri bilinmemektedir. Bu çalışmada bu paramatrelerin OHD’li olan hastalarda düzeyleri ve hastalıkla olan ilişkisi araştırıldı.Materyal ve Metot: Çalışmaya, 0-5 yaş grubu arasında OHD olan hastalar (Çalışma grubu, n=80) ve benzer yaşta sağlıklı çocuklar (Kontrol grubu, n=85) olmak üzere 165 olgu alındı. OHD olan olgular Spina Bifida Occulta (Grup I, n=22), Spinal Meningosel veya Miyelomeningosel (Grup 2, n=26) ve Hidrosefalisi olan (Grup 3, n=31) olmak üzere 3 gruba ayrıldı. Dağılımların normal olup olmadığı tek yönlü Kolmogorov–Smirnov testi ile değerlendirildi. Gruplar arası karşılaştırmalarda, ki-kare, student t testi, Mann-Whitney U testi ve Kruskal-Wallis varyans testleri kullanıldı. Tüm olgularda Fetuin-A ve Osteopontin sandviç enzim bağlantılı immün sistemi emici teknolojiye dayanarak ölçüldü, Total Antioksidan Status (TAS) ve Total Oksidan Status (TOS) spektrofotometrik olarak ölçüldü. TOS’un TAS’a oranıyla oksidatif stres indeksi (OSİ) hesaplandı.Bulgular: Hasta ve kontrol grupları arasında TAS düzeyleri benzerdi (p=0.230). TOS ve OSİ düzeyleri hastalarda, Fetuin-A ve Osteopontin değerleri ise kontrol grubunda daha yüksek bulundu (hepsi için, p<0.05). TAS düzeyleri hasta grupları arasında benzer, TOS, Fetuin-A, Osteopontin değerlerinde anlamlı farklıydı (hepsi için p<0.05). TOS, OSİ ve Fetuin-A düzeyleri grup I den III’e doğru giderek azalırken, osteopontin düzeyleri grup I’de en yüksek, grup 2’de ise en düşük olarak bulundu. Sonuç: OHD kapanma defekti, intrauterin dönemde meydana gelir. Embriyogenez aşamasında, ektodermal tabakadan gelişen nöral dokunun ve mezodermal tabakadan gelişen ve spinal kordun etrafını saran kemik ve cildin orta hatta yetersiz kapanması ile sonuçlanan bir malformasyondur. Bu yetersiz kapanma nöral tüpün herhangi bir yerinde meydana gelebilir. Nöral tüpün histogenezi ve organogenezi tamamlanması için biyolojik ve kimyasal aktif maddelere ihtiyaç duyarlar (2). Bu nedenle OHD’li hastaların fizyopatolojisinde, TOS, OSİ, Fetuin-A, Osteopontin değerlerinin rolü olabileceği düşünülmektedir.

Verrucous Epidermal Nevus: Dermoscopy, Reflectance Confocal Microscopy, and Histopathological Correlation.

Citation: VerzAE, Lacarrubba F, Quattrocchi E, Micali G. Verrucous epidermal nevus: dermoscopy, reflectance confocal microscopy, and histopathological correlation. Dermatol Pract Concept.2019;9(3):230-231. DOI: https://doi.org/10.5826/dpc.0903a16

Defecation by the ctenophore Mnemiopsis leidyi occurs with an ultradian rhythm through a single transient anal pore

AbstractDefecation in the ctenophore Mnemiopsis leidyi is a stereotyped sequence of effector responses that occur with a regular ultradian rhythm. Here I used video microscopy to describe new features and correct previous reports of the gastrovascular system during and between defecations. Contrary to the scientific literature, individuals defecated through only one of the two anal canals which possesses the only anal pore. The anal pore was not visible as a permanent structure as depicted in textbooks, but appeared at defecation and disappeared afterward. Time intervals between repeated defecations in individual animals depended on body size, ranging from ~10 min in small larvae to ~1 hr in large adults. Differential interference contrast microscopy revealed that both the opening and closing of the anal pore resembled a reversible ring of tissue fusion between apposed endodermal and ectodermal layers at the aboral end. Individuals of M. leidyi thus appear to have an intermittent anus and therefore an intermittent through‐gut that reoccur at regular intervals. The temporality of a visible anal pore in M. leidyi is novel, and may shed light on the evolution of a permanent anus and through‐gut in animals. In addition, mirror image dimorphism of the diagonal anal complex occurs in larval ctenophores but not in adults, indicating developmental flexibility in diagonal symmetry of the anal complex.