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PubMed2001

Chromatin reorganization during spermiogenesis of the mollusc Thais hemostoma (Muricidae): implications for sperm nuclear morphogenesis in cenogastropods.

Thais is a cenogastropod mollusc belonging to the Muricidae family. The sperm nuclear morphogenesis of Thais develops in two well-defined and peculiar steps. In the first one, the round early spermatidyl nucleus is penetrated by an endonuclear channel, which arranges as a helix at the inner nuclear surface and organizes the condensing chromatin all around. In the second step, the spiral channel stretches, dragging along the associated chromatin and leading to a definitive cylinder-shaped sperm nucleus. Simultaneously with these changes in nuclear shape, the chromatin is sequentially organized in granules, fibres, lamellae, and, finally, in a very condensed structure, whereas the spermiogenic DNA-associated proteins become more basic and simple. The sperm nucleus contains a small group of protamines consisting of only four types of amino acid (lysine, arginine, glycine, and serine). The most remarkable fact on nuclear spermiogenesis in Thais is that, whereas the chromatin condensation process, the nuclear proteins, and the final shape of sperm nucleus are very similar to those in other muricidae studied, the pathway of nuclear morphogenesis is completely different. We propose an independent genetic control for those two spermiogenic events (chromatin condensation and nucleomorphogenesis). Finally we discuss briefly the main traits of nucleomorphogenesis of muricid molluscs.

Amino Acid Sequence↗
PubMed2000

Mechanisms regulating norgestomet inhibition of endometrial gland morphogenesis in the neonatal ovine uterus.

In many species, endometrial gland adenogenesis occurs neonatally in an ovary- and steroid-independent manner. Chronic exposure of the developing neonatal ovine uterus to norgestomet (NOR) from birth permanently ablates endometrial gland morphogenesis or adenogenesis, creating an adult ovine uterine gland knockout (UGKO) phenotype. This study was conducted to determine the mechanism(s) whereby NOR inhibits adenogenesis in the neonatal ewe. Ewe lambs received no implant or a NOR implant at birth and on postnatal day (PND) 14, and they were necropsied on PND28. Histological analyses of the tracts indicated NOR exposure specifically inhibited endometrial adenogenesis, but no histoarchitectural differences were observed in the oviduct, cervix, or vagina. No effect of NOR treatment was detected on proliferating cell nuclear antigen (PCNA) expression in the endometrial luminal epithelium (LE), stroma, or myometrium. In control (CX) ewes, estrogen receptor alpha (ER-alpha) and progesterone receptor (PR) mRNA and protein were expressed strongly in nascent and proliferating glandular epithelium (GE) but were undetected in epithelium of NOR uteri. Expression of c-met and fibroblast growth factor receptor 2IIIb (FGFR2IIIb) mRNA was detected in the LE and GE of CX uteri. In NOR uteri, c-met was expressed in the LE similar to CX uteri, but FGFR2IIIb mRNA levels were lower than in the LE of CX uteri. Uterine hepatocyte growth factor (HGF), the ligand for c-met, and FGFR2IIIb mRNA expression was substantially lower in NOR ewes, but expression of FGF-7 and FGF-10 mRNAs, ligands for FGFR2IIIb, was unaffected. These results indicate that NOR disrupts endometrial adenogenesis by ablating epithelial ER-alpha expression and altering expression of paracrine growth factors and/or receptors involved in epitheliomesenchymal interactions. Likewise, these mechanisms are proposed to be important regulators of normal uterine gland morphogenesis in the neonate.

Animals↗
PubMed1987

Epigenetic rules for expression of cell adhesion molecules during morphogenesis.

From very early developmental times, cell adhesion molecules (CAMs) play key roles in linking cells together and regulating cell movement. By virtue of their capacity to link epithelia and condense mesenchyme, CAMs can act as mechanochemical regulators of morphogenesis. In the vertebrate species examined so far, CAMs appear in ordered sequences on cell surfaces during development. In this paper, evidence is reviewed indicating that the sequential expression of CAMs on cell surfaces at a variety of sites of embryonic induction follows a set of modulation rules that are first discernible at early gastrulation. These rules are related to the adhesion of cells in collectives and to the establishment of borders between such collectives. After gastrulation, all mesenchymal conversions employ N-CAM and show changes in its prevalence in a transition N----0----N where 0 means low or undetectable amounts of the CAM (rule I). In contrast, epithelia modulate from a state in which N-CAM and L-CAM appear simultaneously to the expression of only one or the other of these primary CAMs (rule II). At a variety of induction sites, cell collectives obeying rule I are found in proximity to cell collectives obeying rule II. During the morphogenesis of complex structures such as the feather or the optic placode, one can see a recursive application of these rules, reflecting the formation of significant histological boundaries within which the expression of gene products other than CAMs can lead to great morphological diversity. It is suggested that the genes for CAMs are regulated independently from and prior to those specifying intracellular proteins in a given tissue. According to this proposal, the existence of the epigenetic rules governing CAM expression reflects the evolutionary conservation of a key means of establishing tissue and animal form through the mechanochemical regulation of processes such as cell division, movement and death.

Animals↗
PubMed1983

Control of early embryonic heart morphogenesis: a hypothesis.

The early events of looping (rotation and bending) of the embryonic vertebrate heart are deformations. The deformative forces and their regulation are intrinsic to the heart. A model of cardiac morphogenesis is described in this paper. It is proposed that synthesis of extracellular matrix by the myocardium generates an internal pressure. This pressure acts as a deforming force on the myocardium which controls strain by regulating compliance. This model provides an explanation of cardiac morphogenesis at the biochemical and biomechanical levels.

Animals↗
PubMed1984

Remodelling of the basement membrane: morphogenesis and maturation.

We have analysed the reciprocal interactions between mouse embryo submandibular epithelium and mesenchyme which result in branching morphogenesis of the epithelium. The interactions modify the composition and metabolism of the basal and reticular laminae which comprise the basement membrane lying between these tissues. The mesenchyme remodels the basement membrane by depositing a type I collagen-rich matrix on the basal lamina and by producing a neutral hyaluronidase, which degrades hyaluronate and chondroitin sulphate, components of this basal lamina. By analogy with mouse mammary epithelial cells, the submandibular epithelial cells have a heparan sulphate-rich proteoglycan on their cell surfaces which is anchored to the cells. The extracellular domain of this integral membrane proteoglycan binds to interstitial collagen. Interfering with the collagen-proteoglycan interaction appears to reduce the morphological stability of the cells. Together with other processes, including epithelial cell proliferation, this remodelling leads to branching epithelial morphogenesis. Basement membrane remodelling may be a general process for regulating cell behaviour during development and is one of the mechanisms of morphogenetic tissue interaction. Remodelling may also cause maturation of basement membranes from a dynamic state of high turnover in the embryo to their persistence and stability in the adult organism.

Animals↗
PubMed1988

Myocardial cell relationships during morphogenesis in normal and cardiac lethal mutant axolotls, Ambystoma mexicanum.

Sarcomere formation has been shown to be deficient in the myocardium of axolotl embryos homozygous for the recessive cardiac lethal gene c. We examined the developing hearts of normal and cardiac mutant embryos from tailbud stage 33 to posthatching stage 43 by scanning electron microscopy in order to determine whether that deficiency has any effect on heart morphogenesis. Specifically, we investigated the relationships of myocardial cells during the formation of the heart tube (stage 33), the initiation of dextral looping (stages 34-36), and the subsequent flexure of the elongating heart (stages 38-43). In addition, we compared the morphogenetic events in the axolotl to the published accounts of comparable stages in the chick embryo. In the axolotl (stage 33), changes in cell shape and orientation accompany the closure of the myocardial trough to form the tubular heart. The ventral mesocardium persists longer in the axolotl embryo than in the chick and appears to contribute to the asymmetry of dextral looping (stages 34-36) in two ways. First, as a persisting structure it places constraints on the simple elongation of the heart tube and the ability of the heart to bend. Second, after it is resorbed, the ventral myocardial cells that contributed to it are identifiable by their orientation, which is orthogonal to adjacent cells: a potential source of shearing effects. Cardiac lethal mutant embryos behave identically during these events, indicating that functional sarcomeres are not necessary to these processes. The absence of dynamic apical myocardial membrane changes, characteristic of the chick embryo (Hamburger and Hamilton stages 9-11), suggests that sudden hydration of the cardiac jelly is less likely to be a major factor in axolotl cardiac morphogenesis. Subsequent flexure (stages 38-43) of the axolotl heart is the same in normal and cardiac lethal mutant embryos as the myocardial tube lengthens within the confines of a pericardial cavity of fixed length. However, the cardiac mutant begins to exhibit abnormalities at this time. The lack of trabeculation (normally beginning at stage 37) in the mutant ventricle is evident at the same time as an increase in myocardial surface area, manifest in extra bends of the heart tube at stage 39. Nonbeating mutant hearts (stage 41) have an abnormally large diameter in the atrioventricular region, possibly the result of the accumulation of ascites fluid. In addition, mutant myocardial cells have a larger apical surface area compared to normals.

Ambystoma↗
PubMed1994

Dynamic expression patterns of tenascin, proteoglycans, and cell adhesion molecules during human hair follicle morphogenesis.

The development of skin appendages such as hair, feathers, and teeth is brought about by reciprocal interactions between epidermal and mesenchymal tissues and is thought to be influenced in part by cell adhesion molecules and components of the extracellular matrix. The developmental distributions of tenascin, neural cell adhesion molecule (NCAM), E-cadherin, intercellular adhesion molecule 1 (ICAM-1), chondroitin sulfate proteoglycan (CSPG), and the heparan sulfate proteoglycan perlecan were studied in relation to hair follicle morphogenesis in fetal human skin. Tenascin first appeared in developing skin in focal concentrations at the epidermal-mesenchymal interface, just prior to, and presumably correlated with, hair follicle initiation. Tenascin immunostaining remained prominent in the basement membrane zone and extracellular matrix of the follicle sheath during subsequent morphogenetic stages. Two forms of tenascin (M(r) 250 x 10(3) and 280-300 x 10(3)), were revealed by Western blots of skin extracts. NCAM immunolabeling was initially present throughout the dermis, and became progressively restricted to the dermal condensation and the follicle sheath. Western blot analysis revealed an isoform of NCAM (M(r) 160 x 10(3)) which lacked polysialic acid. At all stages, E-cadherin staining was diminished on follicle cells situated adjacent to the basement membrane, relative to cells in the follicle interior. Follicle-specific immunostaining for ICAM-1 was transient, appearing only at the pre-germ and hair germ stages of development. Antibodies to three distinct CSPG determinants revealed unique immunolabeling patterns following follicle initiation: One CSPG epitope co-distributed with tenascin in the follicle basement membrane and follicle sheath extracellular matrix; one CSPG epitope was similarly expressed, and was also found on follicle epithelial cells; and the third CSPG determinant was noticeably absent from the follicle sheath during elongation of the developing appendage. Perlecan was concentrated in the dermal papilla, in addition to its distribution in all skin basement membranes. A model for how these diverse molecules may interact to influence human hair follicle morphogenesis is presented.

Blotting, Western↗
PubMed2003

Conjoined twins: morphogenesis of the heart and a review.

Five cases of conjoined twins have been studied. These included three thoracopagus twins, one monocephalus diprosopus (prosop = face), and one dicephalus dipus dibrachus. The thoracopagus twins were conjoined only from the upper thorax to the umbilicus with a normal foregut. These three cases shared a single complex multiventricular heart, one with a four chambered heart with one atrium and one ventricle belonging to each twin with complex venous and arterial connection; two had a seven chambered heart with four atria and three ventricles. The mono-cephalus diprosopus twins had a single heart with tetralogy of Fallot. The dicephalus twins had two separate axial skeletons to the sacrum, two separate hearts were connected between the right atria with a shared inferior vena cava. Thoracopagus twinning is associated with complex cardiac malformations. The cardiac anlagen in cephalopagus or diprosopus are diverted and divided along with the entire rostral end of the embryonic disc and result in two relatively normal shared hearts. However, in thoracopagus twins the single heart is multiventricular and suggests very early union with fusion of the cardiac anlagen before significant differentiation. Cardiac morphogenesis in conjoined twins therefore appears to depend on the site of the conjoined fusion and the temporal and spatial influence that determines morphogenesis as well as abnormally oriented embryonic axes.

Adolescent↗
PubMed1975

Hormonal influences on the morphogenesis of the preputial gland of embryonic mice.

Fetal preputial glands from 14- to 17-day old mouse embryos undergo comparable growth, branching, and display similar degrees of cytodifferentiation when cultured in vitro on medium lacking hormones, on this medium in the presence of either of the fetal gondas, and on medium supplemented with testosterone dipropionate. Conversely, morphogenesis of these analgen is markedly suppressed by estrogen and an anti-androgen, Cyproterone acetate. These observations demonstrate that acquisition of androgen-sensitivity is a late event in the morphogenesis of the preputial gland and correlate with the developmental properties of preputial mesenchyme as demonstrated in earlier studies on the epithelio-mesenchymal interaction.

Animals↗
PubMed1981

Morphogenesis of conjunctival papillae from normal and scaleless chick embryos.

Morphogenesis of avian conjunctival papillae follows a predictable temporal and spatial pattern and is in some manner directly related to the introduction of the underlying scleral ossicles. We have been able, using Scanning Electron Microscopy (SEM), to correlate all of Murray's ('43) histological stages (1--6) of papillae development, with changes in elevation and morphology of the surface of the conjunctiva. The first indication of morphogenesis is the formation of "papillae primordia." The centers of these primordia exhibit decreased intercellular contact, and become elevated as radially symmetrical humps whose surfaces are composed of rounded cells with numerous microvillar projections. As the papillae become asymmetrical and elongate, cells near the tip of the papillae enlarge and develop microridges. During regression of the papillae, single clusters of cells appear to become lost from the surfaces of the papillae into the surrounding fluid. In contrast to normal chick embryos, those homozygous for papillae and underlying scleral ossicles (Palmoski and Goetinck, '70). SEM of the mutant conjunctival surface indicates that these papillae do not exhibit all of Murray's ('43) histological stages and are morphologically abnormal. Data from the present SEM study of the normal and scaleless conjunctiva are discussed in relation to those data of other investigators, and we suggest that Stage 4 in papillae development is critical to scleral ossicle formation.

Animals↗
PubMed2001

Organ formation in Drosophila: specification and morphogenesis of the salivary gland.

The Drosophila salivary gland has emerged as an outstanding model system for the process of organ formation. Many of the component steps, from initial regional specification through cell specialization and morphogenesis, are known and many of the genes required for these different processes have been identified. The salivary gland is a relatively simple organ; the entire gland comprises of only two major cell types, which derive from a single contiguous primordium. Salivary cells cease dividing once they are specified, and organ growth is achieved simply by an increase in size of individual cells, thus eliminating concerns about the potential unequal distribution of determinants during mitosis. Drosophila salivary glands form by the same cellular mechanisms as organs in higher organisms, including regulated cell shape changes, cell intercalation and directed cell migration. Thus, learning how these events are coordinated for tissue morphogenesis in an organism for which the genetic and molecular tools are unsurpassed should provide excellent paradigms for dissecting related processes in the more intricate organs of more complicated species.

Animals↗
PubMed1991

Stabilization of post-translational modification of microtubules during cellular morphogenesis.

This review discusses the possible role of alpha-tubulin detyrosination, a reversible post-translational modification that occurs at the protein's C-terminus, in cellular morphogenesis. Higher eukaryotic cells possess a cyclic post-translational mechanism by which dynamic microtubules are differentiated from their more stable counterparts; a tubulin-specific carboxypeptidase detyrosinates tubulin protomers within microtubules, while the reverse reaction, tyrosination, is performed on the soluble protomer by a second tubulin-specific enzyme, tubulin tyrosine ligase. In general, the turnover of microtubules in undifferentiated, proliferating cells is so rapid that the microtubules accumulate very little detyrosinated tubulin; that is, they are enriched in tyrosinated tubulin. However, an early event common to at least three well-studied morphogenetic events--myogenesis, neuritogenesis, and directed cell motility--is the elaboration of a polarized array of stable microtubules that become enriched in detyrosinated tubulin. The formation of this specialized array of microtubules in specific locations in cells undergoing morphogenesis suggests that it plays an important role in generating cellular asymmetries.

Carboxypeptidases↗
PubMed1995

The making of a fly leg: a model for epithelial morphogenesis.

Epithelial development dictates the shape of an organism. The metamorphic development of a Drosophila leg precursor into an adult leg is a well-defined example of epithelial morphogenesis that can be analyzed from the perspectives of genetics and molecular and cell biology. The steroid hormone 20-hydroxyecdysone induces and regulates the entire process. Mutants affecting Drosophila leg morphogenesis characteristically have short thick legs (the malformed phenotype) resulting from a failure to execute normal cell shape changes at a specific stage of development. Mutations that cause the malformed phenotype have already led to the identification and cloning of genes encoding transcription factors, a transmembrane serine protease presumably required for modification of the apical extracellular matrix, and components of the contractile cytoskeleton and adherens junctions. All of these products are required for the execution of normal changes in leg cell shape.

Animals↗
PubMed2005

Engineering hepatocellular morphogenesis and function via ligand-presenting hydrogels with graded mechanical compliance.

In order to evaluate the sensitivity of hepatocellular cultures to variations in both substrate stiffness and bioactive ligand presentation, hepatocytes were cultured on differentially compliant polyacrylamide gel discs functionalized with varying amounts of the ECM ligand, fibronectin (FN). Subconfluent cell cultures were established in a multiwell plate format enabling the systematic evaluation of cellular response to both underlying substrate rigidity and substrate ligand concentration. Hepatocellular morphogenesis, regulated by a combination of both ligand density and substrate compliance, resulted in a broad spectrum of patterns of cellular reorganization and assembly ranging from highly two-dimensionally spread cells to highly compact, three-dimensional spheroids. Cell compaction was promoted by increasing levels of substrate mechanical compliance and generally inhibited by increasing concentrations of substrate-bound FN. We identified regimes of substrate compliance in which cells are highly responsive or relatively insensitive to the level of substrate-based ligands. For example, while FN presentation did not have a large impact on cell morphogenesis for cultures on highly compliant gels (G' = 1.9 kPa), hepatocytes on "firm" substrates of intermediate compliance (G' = 5.6 kPa) exhibited approximately a 2-fold increase in cell area between the highest and lowest FN concentrations used in this study. Further, we show that increasing substrate compliance at constant ligand concentration results in increased levels of liver-specific albumin secretion while increasing levels of FN at constant substrate rigidity yield reduced liver-specific functional activity. These substrate-elicited differences in cell function also coincided with analogous changes in the transcript levels of metabolic, growth-related, and liver-specific gene markers. Notably, these results also demonstrated that "firm" gel substrates elicit the most hepatocyte functional sensitivity to substrate-based FN presentation. Overall, our findings indicate that hepatocellular responsiveness to ligand concentration can be acutely regulated by gradation of substrate compliance, suggesting that concerted biochemical and biophysical design strategies may be critical toward the fabrication of hepatospecific biomaterials that effectively support desired levels of liver-specific function.

Animals↗
PubMed1988

Maturation of rat visual cortex: IV. The generation, migration, morphogenesis, and connectivity of atypically oriented pyramidal neurons.

The generation, migration, and morphogenesis of atypically oriented pyramidal neurons in the rat visual cortex were examined. In the mature cortex, these neurons were distributed through layers II-VI. Moreover, the atypically oriented pyramidal neurons in a particular layer tended to be oriented in a specific way; atypically oriented pyramidal neurons in layer II, layers III-VIa, and layer VIb were obliquely, radially, and obliquely oriented, respectively. Ultrastructurally, the somata of atypically oriented pyramidal neurons contained large euchromatic ovoid nuclei and cytoplasm that was replete with rough endoplasmic reticulum and Golgi apparatus. These somata formed only symmetric axosomatic synapses. Many atypically oriented pyramidal neurons projected axons into the white matter as demonstrated by a Golgi method and by a retrograde tract-tracing technique; however, some of these pyramidal neurons in layers III-V had axons that ascended to layer I. By using a technique which combined retrograde tract tracing with [3H]thymidine autoradiography, it was determined that most atypically oriented pyramidal neurons in layers V and VIa, layer IV, and layer II were generated on gestational days (GD) 15-17, GD 17-19, and GD 20-21, respectively. Atypically oreinted pyramidal neurons were identified during the period from postnatal day 0 (day of birth) to day 30. On day 0, obliquely oriented pyramidal neurons were distributed in the deep cortical plate, i.e., immature layer VI. On day 3, the youngest atypically oriented pyramidal neurons were radially oriented and were located in layer IV. Some obliquely oriented pyramidal neurons were present in layer II on day 6, but the greatest number and the most severely canted pyramidal neurons in layer II were evident on day 9. The orientations of the cell body and the apical dendrite did not change appreciably after migration was complete, except for those in layers V and VI with obliquely oriented cell bodies and radially oriented apical dendrites. The second and third postnatal weeks were marked by substantial morphological differentiation of all pyramidal neurons as noted by the lengthening and branching of dendrites and by the appearance of dendritic spines. By the fourth postnatal week, atypically oriented pyramidal neurons achieved their mature morphology. The generation, migration, and morphogenesis of atypically oriented pyramidal neurons proceed by an inside-to-outside sequence. This development is similar and concurrent with that of typically oriented pyramidal neurons.

Aging↗
PubMed2002

PDGF-A/PDGF alpha-receptor signaling is required for lung growth and the formation of alveoli but not for early lung branching morphogenesis.

Platelet-derived growth factors (PDGF) constitute a family of four gene products (PDGF-A-D) acting by means of two receptor tyrosine kinases, PDGFR alpha and beta. Three of the ligands (PDGF-A, -B, and -C) bind to PDGFR alpha with high affinity. Knockout of pdgf-a in mice has demonstrated a role for PDGF-A in the recruitment of smooth muscle cells to the alveolar sacs and their further compartmentalization into alveoli. Although this is a late, postnatal step in lung development, pdgf-a antisense oligonucleotides were previously shown to inhibit epithelial branching in rat lung explants in vitro, which reflects an early embryonic process. These conflicting results may be explained by substitution of genetic loss of pdgf-a by maternal transfer of PDGF-A to the knockout embryo or the presence of other PDGFR alpha agonists (PDGF-B and -C) in vivo, potentially masking an effect of PDGF-A on branching morphogenesis. Alternatively, the administration of pdgf-a antisense oligonucleotides affected other processes than the intended. To discriminate between these opposing possibilities, we have analyzed lung development in pdgfr alpha -/- embryos and lung primordia grown in vitro. Our analysis shows that, while the pdgfr alpha -/- lungs and explanted lung rudiments were smaller than normal, branching morphogenesis appears qualitatively intact and proceeds until at least embryonic day 15.5, generating both prospective conducting and respiratory airways. We conclude that, although PDGF-AA signaling over PDGFR alpha may have direct or indirect roles in overall lung growth, it does not specifically control early branching of the lung epithelium.

Animals↗
PubMed2004

Role of cranial neural crest cells in visceral arch muscle positioning and morphogenesis in the Mexican axolotl, Ambystoma mexicanum.

The role of cranial neural crest cells in the formation of visceral arch musculature was investigated in the Mexican axolotl, Ambystoma mexicanum. DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine, perchlorate) labeling and green fluorescent protein (GFP) mRNA injections combined with unilateral transplantations of neural folds showed that neural crest cells contribute to the connective tissues but not the myofibers of developing visceral arch muscles in the mandibular, hyoid, and branchial arches. Extirpations of individual cranial neural crest streams demonstrated that neural crest cells are necessary for correct morphogenesis of visceral arch muscles. These do, however, initially develop in their proper positions also in the absence of cranial neural crest. Visceral arch muscles forming in the absence of neural crest cells start to differentiate at their origins but fail to extend toward their insertions and may have a frayed appearance. Our data indicate that visceral arch muscle positioning is controlled by factors that do not have a neural crest origin. We suggest that the cranial neural crest-derived connective tissues provide directional guidance important for the proper extension of the cranial muscles and the subsequent attachment to the insertion on the correct cartilage. In a comparative context, our data from the Mexican axolotl support the view that the cranial neural crest plays a fundamental role in the development of not only the skeleton of the vertebrate head but also in the morphogenesis of the cranial muscles and that this might be a primitive feature of cranial development in vertebrates.

Ambystoma mexicanum↗
PubMed2005

Genetic locus half baked is necessary for morphogenesis of the ectoderm.

The zebrafish epiboly mutants partially block epiboly, the vegetalward movement of the blastoderm around the giant yolk cell. Here, we show that the epiboly mutations are located near the centromere of Linkage Group 7 in a single locus, termed the half baked locus. Nevertheless, except for the similar mutants lawine and avalanche, we find the epiboly traits of each of the alleles to be distinguishable, forming an allelic series. Using in situ analysis, we show that the specification and the formation of the germ layers is unaffected. However, during early gastrulation, convergence movements are slowed in homozygous and zygotic maternal dominant (ZMD) heterozygous mutants, especially in the epiblast layer of the blastoderm. Using triple-mutant analysis with squint and cyclops, we show that ablating involution and hypoblast formation in hab has no effect on the epiboly phenotype on the ventral and lateral sides of the embryo, suggesting that the hypoblast has no role in epiboly. Moreover, the triple mutant enhances the depletion of cells on the dorsal side of the embryo, consistent with the idea that convergence movements are defective. Double-mutant analysis with one-eyed pinhead reveals that hab is necessary in the ectodermal portion of the hatching gland. In ZMD heterozygotes, in addition to the slowing of epiboly, morphogenesis of the neural tube is abnormal, with gaps forming in the midline during segmentation stages; later, ectopic rows of neurons form in the widened spinal cord and hindbrain. Cell transplantation reveals that half baked acts both autonomously and nonautonomously in interactions among cells of the forming neural tube. Together, these results suggest that half baked is necessary within the epiblast for morphogenesis during both epiboly and neurulation and suggest that the mechanisms that drive epiboly possess common elements with those that underlie convergence and extension.

Alleles↗