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PubMed1999

Membrane-bound transferrin-like protein (MTf): structure, evolution and selective expression during chondrogenic differentiation of mouse embryonic cells.

Mouse membrane-bound transferrin-like protein (MTf) cDNA was cloned to examine its expression during chondrogenic differentiation in the mouse embryonic cell line ATDC5, and to analyze the phylogenetic relationships among the MTfs of four animal species and 23 other transferrin members. Phylogenetic analysis indicated that the MTf gene diverged from the common ancestor gene earlier than the genes of the other transferrins such as serum transferrin, lactoferrin and ovotransferrin, and that the divergence occurred after the divergence of vertebrates and invertebrates. MTf, as well as the other transferrins, consists of two repeated domains. The similarity between the N-terminal and the C-terminal domains of MTf is much higher than that of the other transferrins, although the five amino acid residues required for iron binding were not conserved in the C-terminal domain of MTf in contrast to the conservation of these residues in both domains of the other transferrins. Among various adult mouse tissues, MTf mRNA was expressed at the highest level in cartilage and at a moderate level in the testis. MTf mRNA was expressed only at very low levels in the brain, spleen, thymus, muscle, lung, skin and intestine, and hardly detected in the heart, kidney, stomach and liver. In cultures of the mouse ATDC5 cell line, MTf is developmentally expressed in parallel with the expression of type II collagen and aggrecan, in the pattern commensurate with the onset of chondrogenesis to form cartilage nodules. The structural characteristics and the expression pattern suggest that during development and in adult tissues, MTf has some functions that are different from those of other transferrins.

Amino Acid Sequence↗
PubMed2000

Distinct roles of the homeotic genes Ubx and abd-A in beetle embryonic abdominal appendage development.

Insects are easily distinguishable by the absence of legs on the adult abdomen. Studies performed on the Dipteran, Drosophila melanogaster, indicate that this is because of the repressive effects of the homeotic genes Ultrabithorax (Ubx) and abdominal-A (abd-A) on the limb promoting gene Distal-less (Dll) during embryonic development. However, in many species appendage-like structures are present on abdominal segments in embryonic and juvenile stages. Here, by using classical genetics and double-stranded RNA-mediated gene silencing in the red flour beetle, Tribolium castaneum, a species that develops an appendage on the first abdominal segment, we investigate the roles of Ubx and Abd-A in abdominal limb development. We find that in Tribolium, Abd-A, but not Ubx, represses early expression of Dll in the embryonic abdomen. Ubx appears to modify the A1 appendage. This difference in the activities of Abd-A and Ubx is critical for proper development of this appendage. We suggest that an ancestral role of Abd-A in insect abdominal appendage development was in the repression of Dll initiation and that of Ubx was in modulation of abdominal appendage morphology.

Abdomen↗
PubMed1975

Cholinesterase in embryonic development.

I. Cholinesterase (ChE) activity was studied histochemically during early development of the sea urchin, the amphibian, the chick and the rat embryo. After formalin fixation and embedding in water-soluble carbowax, the enzyme reaction was carried out in serial section. 2. Independent from innervation ChE appears in every embryonic blastema in a very early stage of development. It disappears from the embryonic cells after they have assembled into definite organ structures. Thus, ChE plays a role in embryonic development which is different from its known function in the adult. Therefore, ChE activity present in differentiating cells during a limited phase of development, is termed "embryonic cholinesterase". 3. Embryonic ChE was invariably found in cells engaged in morphogenetic movements. This observation has led us to suppose that the enzyme in involved in the regulation of cellular movements during development. 4. In particular, embryonic ChE is described in the following locations: a) During sea urchin gastrulation ChE is present in the primary mesenchymal cells emigrating from the blastula wall and in the archenteron cells which are known to bring about the invagination movement by contraction of their pseudopods. b) In the early chick blastoderm ChE active "droplet cells" are described which are supposed to emigrate from the epiblast layer in order to form the hypoblast. c) During development of notochord and somites, during closure of the neural tube and development of the head anlage, the close correlation of ChE activity with various morphogenetic movements is demonstrated: ChE appears during aggregation and desaggregation of epithelial compounds. The active bending of preexisting epithelial sheets, such as the neural plate, is also accompanied by ChE activity in epithelial cells...

Acetylcholinesterase↗
PubMed2001

An alternatively spliced Muc10 glycoprotein ligand for putative L-selectin binding during mouse embryonic submandibular gland morphogenesis.

Late-gestation (embryonic day 18; E18) mouse submandibular glands (SMG) comprise a network of large and small ducts that terminate in lumen-containing, presumptive acini (terminal buds) expressing unique, cell membrane-associated embryonic mucin. The objective here was to clone and sequence embryonic low molecular-weight SMG mucin, predict its secondary structure, and begin to investigate its possible role in SMG development. Evidence was found that: (1) embryonic low molecular-weight mucin is an alternatively spliced Muc10 gene product, 220 amino acids in size (approximately 25 kDa), rich in potential O-glycosylation sites, and variably glycosylated (approximately 40 and 68 kDa); (2) consensus secondary-structure prediction for embryonic low molecular-weight mucin is consistent with a molecule that is anchored to the plasma membrane, directly or indirectly (via a glycolipid), and has a protein core that serves as a scaffold for carbohydrate presentation; (3) embryonic L-selectin is immunolocalized to the plasma membrane region of terminal-bud epithelial cells in a pattern similar to that seen for embryonic mucin; (4) embryonic, but not adult, mucin is able to bind L-selectin and does so endogenously in E18 SMG. As the primary role of L-selectin is to mediate cell adhesion and its ligands are mucin-like glycoproteins, it is suggested that this embryonic low molecular-weight mucin be termed MucCAM.

Age Factors↗
PubMed2003

The Caenorhabditis elegans innexin INX-3 is localized to gap junctions and is essential for embryonic development.

Innexins are the proposed structural components of gap junctions in invertebrates. Antibodies that specifically recognize the Caenorhabditis elegans innexin protein INX-3 were generated and used to examine the patterns of inx-3 gene expression and the subcellular sites of INX-3 localization. INX-3 is first detected in two-cell embryos, concentrated at the intercellular interface, and is expressed ubiquitously throughout the cellular proliferation phase of embryogenesis. During embryonic morphogenesis, INX-3 expression becomes more restricted. Postembryonically, INX-3 is expressed transiently in several cell types, while expression in the posterior pharynx persists throughout development. Through immuno-EM techniques, INX-3 was observed at gap junctions in the adult pharynx, providing supporting evidence that innexins are components of gap junctions. An inx-3 mutant was isolated through a combined genetic and immunocytochemical screen. Homozygous inx-3 mutants exhibit defects during embryonic morphogenesis. At the comma stage of early morphogenesis, variable numbers of cells are lost from the anterior of inx-3(lw68) mutants. A range of terminal defects is seen later in embryogenesis, including localized rupture of the hypodermis, failure of the midbody to elongate properly, abnormal contacts between hypodermal cells, and failure of the pharynx to attach to the anterior of the animal.

Animals↗
PubMed2004

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy.

Nitric oxide (NO) has been demonstrated to mediate events during ovulation, pregnancy, blastocyst invasion and preimplantation embryogenesis. However, less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development, an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO (L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species (ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

Animals↗
PubMed2001

Bone morphogenetic protein 4 induces efficient hematopoietic differentiation of rhesus monkey embryonic stem cells in vitro.

A cell culture system consisting of mouse S17 stromal cells supplemented with cytokines was developed for hematopoietic differentiation of rhesus monkey embryonic stem (ES) cells. The differentiated colonies that formed contained clusters of hematopoietic-like cells, as well as structures similar in appearance to embryonic blood islands. When this culture system was supplemented with bone morphogenetic protein 4 (BMP-4), the numbers of primary hematopoietic clusters increased by an average of 15 fold. The primary hematopoietic clusters containing clonogenic precursors (expandable hematopoietic clusters) increased by 18 fold. Immunofluorescence analysis showed that a substantial percentage of the hematopoietic-like cells were CD34(+), with morphologic features of undifferentiated blast cells. Enrichment of the CD34(+) cells was associated with enhanced stromal-dependent, cytokine-driven formation of cobblestone colonies on secondary plating. The hematopoietic identity of the precursors was further indicated by their expression of genes associated with hematopoietic differentiation, as well as morphologic assessments that showed erythroid and myeloid lineages among the progeny cells. In addition, reverse transcriptase-polymerase chain reaction analysis of BMP-4-treated rhesus monkey ES cells demonstrated an up-regulation of early-expressed genes responsible for embryonic hematopoiesis and angiogenesis during the first 7 days of culture. These observations suggest that embryonic mesoderm regulatory protein may mimic physiologic signals that are required for the onset of embryonic hematopoiesis and stem cell formation in rhesus monkey ES cells.

Animals↗
PubMed2002

Intracellular Ca2+ store in embryonic cardiac myocytes.

In mature cardiac myocytes, Ca2+ influx through the L-type Ca2+ channel activates the ryanodine receptor and triggers Ca2+ release from the sarcoplasmic reticulum (SR). This Ca2+ signal amplification, termed Ca2+-induced Ca2+ release (CICR), occurs within the junctional membrane complex between the plasma membrane and the SR, and is essential for cardiac excitation-contraction (E-C) coupling. On the other hand, Ca2+ available during E-C coupling is predominantly derived from Ca2+ influx in embryonic cardiac myocytes. To examine the role of the intracellular Ca2+ store in immature cardiac myocytes, we have generated knockout mice lacking the cardiac type of the ryanodine receptor (RyR-2), or junctophilin (JP-2) contributing to formation of the junctional membrane complex. Both RyR-2- and JP-2-knockout mice show lethality at early embryonic stages immediately after beginning of heart beating. The loss of RyR-2 produced abnormal SR elements exhibiting vacuolated structures and Ca2+-overloading in embryonic cardiac myocytes. In JP-2-deficient cardiac myocytes, formation of junctional membrane complexes, called pheripheral couplings, was disturbed, and abnormal Ca2+ transients without spatial and temporal synchronization were observed. Therefore, the knockout mice have demonstrated that RyR-2-mediated Ca2+ release at the junctional membrane complex is essential for cellular Ca2+ homeostasis in immature cardiac myocytes.

Animals↗
PubMed2003

TNF-alpha acts to prevent occurrence of malformed fetuses in diabetic mice.

AIMS/HYPOTHESIS: Activation of apoptosis in embryos is thought to be a key event in the pathogenesis of diabetes-induced embryopathies such as early embryonic death and inborn structural anomalies. TNF-alpha can activate apoptotic and anti-apoptotic signalling cascades, indicating its ability to contribute to and counteract diabetes-induced maldevelopment. To investigate how TNF-alpha regulates the response of embryos to diabetes-induced embryopathic stress, we used streptozotocin-induced diabetic TNF-alpha knockout mice. MATERIALS: To evaluate the reproductive performance, mated diabetic female mice were examined on days 4 and 8 of pregnancy for the presence of blastocysts or embryos in uterine horns. To evaluate the teratogenic effect, the female mice were killed on day 18 of pregnancy and fetuses were examined for gross external anomalies. In addition, apoptotic nuclei were localised by the TUNEL assay and DNA-binding activity of the transcription factor NF-kappaB was evaluated by electrophoretic mobility shift assay in 10- and 11-day-old embryos respectively. RESULTS: Severely diabetic TNF-alpha(+/+) female mice had a much greater decrease in pregnancy rate but a lower incidence of malformed fetuses in litters than severely diabetic TNF-alpha(-/-) female mice. Also, the intensity of excessive apoptosis was higher, but the amount of active NF-kappaB complexes was lower in malformed TNF-alpha(-/-) embryos than in TNF-alpha(+/+) embryos. CONCLUSIONS/INTERPRETATION: TNF-alpha contributes to death of peri-implantation embryos and possibly protects postimplantation embryos exposed to diabetes-induced teratogenic stimuli via activation of NF-kappaB-mediated anti-apoptotic signalling. It seems that TNF-alpha prevents the birth of malformed offspring in severely diabetic mice.

Animals↗
PubMed1992

Embryonic development of the CNS microvasculature in the mouse: new insights into the structural mechanisms of early angiogenesis.

Vascularization and expression of blood-brain barrier (bbb) associated morphological characteristics were studied by ultrastructural analysis during the embryonic development of the mouse CNS. At day 9 (E9) capillaries were only found in the perineural mesenchymal tissue exhibiting fenestrations and loosely attached pericytes. At E10 endothelial cells (EC) together with pericytes and other mesenchymal cells invaded the intraneural domain. The immigrating EC showed numerous protrusions and lost their fenestrations as soon as the new intraneural capillaries were formed. Intraneural EC showed prominent nuclei, many pinocytotic vesicles and junctional complexes which appeared tight in some places. These results indicate that from the first day of intraneural vascularization onwards, the morphological properties of the bbb are present in the early embryonic mouse cerebral cortex.

Animals↗
PubMed1980

Characterization of a human ovarian teratocarcinoma-derived cell line.

A cell line (PA I), derived from human ovarian teratocarcinoma cells, was obtained by culturing ascitic fluid cells from a patient with recurrence of malignant ovarian teratoma. During early passages the cultured cells showed a variable morphology, a long doubling time, and a low plating efficiency (2%). After about 50 passages in vitro, a cell population which was more homogeneous and resembled embryonal carcinoma cells were obtained. These cells had a shorter doubling time (26 h), and increased plating efficiency (77%). The early-passage cells were aneuploid (P 24) whereas the late-passage cells had a normal diploid karyotype with one balanced translocation between chromosomes No. 15 and No. 20 (P 224). Details of the karyotype suggest that the cells are heterozygous, i.e. derived from a stage before the first meiotic division. One of the two X chromosomes were inactive, and the cells expressed HLA antigens (A28 and B12), and beta 2-microglobulin. Expression of F9 antigen, characteristic of two-cell and later preimplantation embryos, was absent, while expression of PCC4 antigen, expressed also by blastocysts, was present. This finding suggests that the line might express some embryonic characteristics. The PA I cell line maintained in monolayer cultures showed several characteristics of malignant cells. The proportion of malignant cells increased with successive passages in vitro. The late-passage cells represented a fairly homogenous population of malignant cells similar to embryonal carcinoma cells. Late-passage PA I cells, when seeded under conditions that prevented attachment of cells to the substratum, formed embryoid bodies consisting of an inner core of cells similar to embryonal carcinoma cells, surrounded by a rind of endoderm-like cells. These two cell layers were separated by a basement membrane-like structure containing fibronectin. The core embryonal carcinoma cells expressed high alkaline phosphatase activity whereas the endoderm-like cells had low alkaline phosphatase activity. Embryoid bodies seeded on an adhesive substratum formed polycystic structures divided by layers of epithelial-like cells and containing extracellular fibrils similar to collagen type I or III. In these cultures, further limited differentiation into endoderm-like, epithelial-like cells and pigmented cells was observed. Morphological differenciation of undifferentiated PA I cells into endoderm-like cells in monolayer cultures could be obtained by treatment with BrdUrd or by plating in low serum concentration and at low density. Cells with characteristic fibrillar distribution of fibronectin and actin microfilament bundles were then observed, indicating formation of cells lacking properties of malignant cells. As indicated by these results, the PA I cell line, in spite of a limited capacity to differentiate in vitro, shares some of the properties of mouse teratocarcinoma cell lines and might therefore serve as a useful model for studies on some developmental mechanisms in human cells.

Antigens, Surface↗
PubMed2005

Osteogenic differentiation within intact human embryoid bodies result in a marked increase in osteocalcin secretion after 12 days of in vitro culture, and formation of morphologically distinct nodule-like structures.

Osteogenic lineages derived from human embryonic stem cells hold much promise for clinical application in bone regeneration, in addition to providing a useful research model in developmental biology, and for pharmacological and cytotoxicity screening of bone-related biomaterials and drugs in vitro. Previously, osteogenic differentiation of human embryonic stem cells was achieved through dissociation of embryoid bodies by trypsinization, prior to culture with osteogenesis-promoting medium. This study therefore attempted a new approach: that is to achieve osteogenesis within intact human embryoid bodies. After 22 days of culture in osteogenesis-promoting medium comprising a cocktail of ascorbic acid, beta-glycerophosphate and dexamethasone, the attached embryoid bodies exhibited much cellular outgrowth and migration, and formed morphologically distinct nodule-like structures. These were somewhat similar to osteogenic nodules formed by mesenchymal stem cells, as reported by previous studies. Immunohistochemical staining and RT-PCR analysis confirmed the presence of osteogenic cells within these nodule-like structures. Additionally, the quantitative assay of osteocalcin secretion demonstrated a rapid sharp increase in osteocalcin expression on day 12 of in vitro culture, which could suggest the appearance of differentiated osteoblasts from day 12 onwards. Future work will attempt to investigate whether other cytokines, growth factors and chemical compounds could further enhance osteogenesis within intact human embryoid bodies.

Ascorbic Acid↗
PubMed1999

Establishing homology criteria for regulatory gene networks: prospects and challenges.

One of the most remarkable discoveries to emerge from the field of developmental genetics is the observation that many regulatory genes and segments of their interactive networks (pathways) appear to have been conserved in several metazoan phyla. Determining whether these conserved regulatory networks are homologous, i.e. derived from an equivalent network in the most recent common ancestor, is critical to understanding comparisons between model system studies, and the evolution of metazoan body plans. To this end, I outline some of the evolutionary properties of regulatory networks, and propose both similarity and phylogenetic criteria that can be used to test the hypothesis that two regulatory networks are homologous. Furthermore, I propose that genetic networks can be treated as a distinct level of biological organization, and can be analysed together with other hierarchical levels, such as genes, embryonic origins and morphological structures, in a comparative framework. Examples from the literature, particularly the genetic regulatory networks involved in patterning arthropod and vertebrate limbs, are examined using the proposed criteria and hierarchical approach.

Animals↗
PubMed1986

Occurrence of holoprosencephaly in chromosome 13 disorders cannot be explained by duplication/deficiency of a single locus.

Four cases of holoprosencephaly with duplication/deletion involving chromosome 13 are presented and additional cases are summarized from the literature. When examined as a series, the duplications (trisomy 13, trisomy 13pter----q14) and deletions (deletion 13q12----qter, deletion 13q31----qter, ring 13 with deletion 13q14----qter) exclude deletion or duplication of single chromosome 13 bands as the cause for holoprosencephaly. Increased dosage of the 13pter----q14 region relative to the 13q14----qter region as the cause is also ruled out by the duplication 13q21----qter cases reported in the literature. Altered timing of forebrain development, causing reversion to a more primitive embryonic and phylogenetic brain structure, is related to dosage imbalance of at least two chromosome 13 regions.

Chromosome Aberrations↗
PubMed2005

EGF-R and erbB-2 in murine tooth development after ethanol exposure.

BACKGROUND: Alcohol consumption during pregnancy can frequently lead to a congenital disorder known as fetal alcohol syndrome (FAS); however, not all children born to alcoholic women develop FAS. Alcohol consumption may affect diverse organs and systems during embryonic development, including craniofacial structures. Small teeth, enamel alterations, and delayed eruption have been observed after ethanol exposure. Epidermal growth factor receptors (EGF-Rs) participate in dental proliferation and differentiation, and changes in these receptors were considered here to be a likely mechanism associated to the dental anomalies observed in this syndrome. Epidermal growth factor receptor type 1 (EGF-R) and epidermal growth factor receptor type 2 (erbB-2) immunoexpression during the lower first molar morphogenesis was investigated in mouse fetuses exposed to ethanol during gestation. METHODS: Pregnant female mice were divided into groups, consuming either 5, 10, 15, 20, or 25% ethanol solutions, or water (control group). Heads were obtained from 16.5- and 18.5-day fetuses. Immunohistochemistry was applied to EGF-R and erbB-2. RESULTS: At days 16.5 and 18.5, fetuses from 15%, 20%, and 25% ethanol groups showed delayed differentiation, degenerative changes in dental epithelial tissues and reduced dental size; additionally, they displayed an enhanced immunoreactivity to EGF-R and erbB-2. CONCLUSIONS: Our results suggest that ethanol consumption during pregnancy affects the expression of EGF receptors and induces a delay in murine fetal dental morphogenesis. Dental development is a process that involves a number of growth factors; hence we consider that further research is required to show whether the changes in glycosylation and growth-factor signaling pathways observed in other cells are also involved in the alterations observed in this study.

Animals↗
PubMed1981

3H-thymidine autoradiographic analysis of telencephalic histogenesis in the chick embryo: I. Neuronal birthdates of telencephalic compartments in situ.

The birthdates of neuronal populations comprising the chick telencephalon were determined by 3H-thymidine labeling and were mapped with respect to their terminal positions in the 16-day embryo. Essentially all neurons were generated between four and nine days of embryonic development. Each telencephalic structure (based on terminology used by Karten and Hodos, '67) was characterized by a specific range of birthdates: some regions such as the core of the ectostriatum or the paleostriatum primitivum, were generated within a single day, while others, such as the hyperstriatum accessorium, required up to five days for generation of the complete population. Spatial-temporal gradients of neuronal birthdates, lateromedial and ventrodorsal, were seen in the telencephalon as a whole and within individual subcompartments as well. An "outside-in" pattern of histogenesis predominated throughout the entire telencephalon, including the dorsolateral cortex. However, notable exceptions pertaining to the paleostriatum augmentatum, hyperstriatum intercalatus and field "L" were observed. Glial cells, generated for the most part after day ten, were found to be distributed homogeneously throughout all areas of the telencephalon. These data provide the first birthdating data for an avian telencephalon and bring greater resolution to previous analyses of the histogenesis of this brain region. Further, the compartmentalization of the proliferative neuroepithelium is revealed by these data, and the possibility of a common time of origin in the neuroepithelium for neurons of related function is discussed.

Animals↗
PubMed1981

Neurite growth promoting factors of embryonic chick--ontogeny, regional distribution, and characteristics.

A single neuronal cell biological assay for NGF has been used to quantitate factors in soluble extract of chick embryo that promote neurite outgrowth. The neurite growth promoting activity is detected as early as day 1.5 of embryonic life. Specific activity increases to maximum over the first four days and then decreases from day 5 to 6 during a growth spurt of the embryo. The tissue distribution of neurite growth promoting activity at eight embryonic days shows higher specific activity in peripheral structures that are richly innervated. Extract from all embryonic stages and from all tissues studied induces neurite outgrowth that is inhibited only partially by antibody to mouse NGF. Furthermore, the kinetics of neurite outgrowth and the neuronal populations responsive to extract differ from that of NGF. These observations indicate heterogeneity of the neurite growth promoting factors in soluble extracts of embryonic chick and demonstrate the presence of these factors before the responsive neurons leave the cell cycle and begin their differentiation processes.

Aging↗
PubMed1993

Two phases in the establishment of HOX expression domains.

Vertebrate HOX genes are thought to play a role in the transmission of anteroposterior (A-P) positional information to the cellular precursors of embryonic axial and paraxial structures. We present an in situ analysis of the expression of two adjacent HOX genes, Hox-2.3 and Hox-2.4. We discuss the data on early gene expression in the light of what is known about cell behavior, cellular fate maps, and A-P regionalization during gastrulation. After the genes are switched on in the most posterior part of the embryo at the late primitive streak stage, the expression domains spread, in a way that does not correlate with cell lineage, toward more cranial positions within and along the streak in mesoderm and ectoderm. A second phase of HOX gene expression takes place at the early somite stage after the expression domains have reached the region around and lateral to the anterior part of the streak (the equivalent of the chicken Hensen's node). HOX gene expression during this second phase is probably clonally transmitted and would be directly associated with the acquisition of A-P positional identity by the progenitors of paraxial mesoderm and neurectoderm which are located anterolaterally to the node.

Animals↗