The behaviour of the egg pigment in wild-type and ‘rusty’ tadpoles of Xenopus laevis

Development ◽  
1971 ◽  
Vol 26 (3) ◽  
pp. 571-585
Author(s):  
V. Uehlinger ◽  
M. L. Beauchemin ◽  
A. Droin
Keyword(s):  
Xenopus Laevis ◽  
Neural Tube ◽  
Histological Analysis ◽  
Exceptional Case ◽  
Cement Gland ◽  
Wild Type ◽  
Specific Process ◽  
Pigment Migration ◽  
Characteristic Colour ◽  
Neurula Stage

The behaviour of the egg pigment was studied by histological analysis of wild-type and ‘rusty’ embryos and tadpoles of Xenopus laevis as well as by experimental procedures. The histological analysis of the wild-type animals showed that the various tissues, notably the skin, neural tube, alimentary system and cement gland go through progressive stages of egg pigment migration and concentration at the apical ends of the cells. In the ‘rusty’ mutants the migration and concentration of pigment occur to a slight extent only, the majority of the pigment granules remaining dispersed. The experiments (tail cultures, squashes of cement gland mucus and of meconium) showed that in wild-type animals the pigment, after migration and concentration, is eliminated from the cells by expulsion. In ‘rusty’ animals, this expulsion does not take place. Parabiotic tadpoles of a ‘rusty’ wild-type combination possess a coloration corresponding to their genotype. Ectodermal grafts performed at the neurula stage between ‘rusty’ and wild-type embryos develop according to their origin. The amount of egg pigment found in wild-type and ‘rusty’ tadpoles, and the exceptional case of the cement gland are discussed. It is concluded that the behaviour of the egg pigment is an active cell-specific process, and that the pigment is eliminated by expulsion. The non-elimination of the egg pigment in the ‘rusty’ mutant, accounting for its characteristic colour, appears to be due to a failure of the expulsion mechanism.

scholarly journals The Ultrastructure of the Cement Gland in Xenopus laevis

1966 ◽  
Vol 1 (2) ◽  
pp. 193-200 ◽  
Author(s):  
MARGARET M. PERRY ◽  
C. H. WADDINGTON
Keyword(s):  
Endoplasmic Reticulum ◽  
Xenopus Laevis ◽  
Secretory Granules ◽  
Progressive Increase ◽  
Cement Gland ◽  
Membrane Systems ◽  
Large Numbers ◽  
Cytoplasmic Filaments ◽  
Golgi Zone ◽  
Neurula Stage

Alterations which occur during differentiation in the fine structure of the cement gland of the embryo of Xenopus laevis have been investigated. The organ anlage at the late neurula stage is composed of cuboidal cells of comparatively simple cytoplasmic structure. Coincident with the subsequent cellular elongation there is a formation of extensive arrays of functionally interrelated membrane systems, leading to the production of a mucin-like secretory substance. Although there is no direct structural continuity between the membranes of the endoplasmic reticulum and the Golgi apparatus, small vesicles which seem to originate from areas of agranular reticulum appear to transport material synthesized in the endoplasmic reticulum to the Golgi zone. Further elaboration of the product at the site of the Golgi material is suggested by the progressive increase in the quantity of the contents as the cisternae enlarge to form secretory granules. Other notable features of the differentiating cells are microtubules and cytoplasmic filaments, many of which are oriented in the direction of cellular elongation. In suitably preserved specimens, large numbers of glycogen granules are present. The degenerating gland is characterized by the appearance of large autolytic vacuoles within the cytoplasm. Traces of the membrane systems are present and, in many cells, there remain large numbers of secretory granules.

Leaflet initiation is temporally and spatially separated in simple and complex tomato (Solanum lycopersicum) leaf mutants: a developmental analysis

Botany ◽  
2010 ◽  
Vol 88 (8) ◽  
pp. 710-724 ◽  
Author(s):  
Julie Kang ◽  
Neelima R. Sinha
Keyword(s):  
Histological Analysis ◽  
Wild Type ◽  
Knox Gene ◽  
Leaf Morphogenesis ◽  
Multiple Factors ◽  
Developmental Program ◽  
Meristematic Activity ◽  
Primary Leaflet ◽  
Developmental Analysis ◽  
Leaf Mutants

Formation of a compound leaf requires the involvement of multiple factors, including KNOX1 gene expression. To further characterize simple and complex tomato leaf mutants, we analyzed their morphology and development by assessing: leaf phenotypes, primary leaf morphogenesis, expression of the class I KNOX gene LeT6, and meristematic activity of the marginal blastozone. Mutants with alterations in lobing and (or) pinnation (decrease/increase) were analyzed. Primary leaflet initiation is delayed in mutants with decreased lobing. In contrast, leaflet initiation is advanced or similar to the wild type in mutants with deep lobes. Leaves with increased pinnation along the rachis require a protracted developmental program to form their final leaf morphology. Using a morphometric analysis, we show that leaf complexity can be quantified. The expression pattern of LeT6 correlates with histological analysis of meristematic activity of the marginal blastozone, suggesting that LeT6 may play a role, through some unknown mechanism, to regulate meristematic competence, not only in the marginal blastozone to regulate leaflet lobing, but along the entire length of the leaf to regulate pinnation in compound leaves.

The fate of cells in the tailbud of Xenopus laevis

Development ◽  
2000 ◽  
Vol 127 (2) ◽  
pp. 255-267 ◽  
Author(s):  
R.L. Davis ◽  
M.W. Kirschner
Keyword(s):  
Xenopus Laevis ◽  
Small Groups ◽  
Neural Tube ◽  
Cell Types ◽  
Similar Distribution ◽  
Germ Layer ◽  
Cell Determination ◽  
Multipotent Cells ◽  
Axial Development

The vertebrate tailbud and trunk form very similar tissues. It has been a controversial question for decades whether cell determination in the developing tail proceeds as part of early axial development or whether it proceeds by a different mechanism. To examine this question more closely, we have used photoactivation of fluorescence to mark small neighborhoods of cells in the developing tailbud of Xenopus laevis. We show that, in one region of the tailbud, very small groups of adjacent cells can contribute progeny to the neural tube, notochord and somitic muscle, as well as other identified cell types within a single embryo. Groups averaging three adjacent cells at a later stage can contribute progeny with a similar distribution. Our data suggest that the tailbud contains multipotent cells that make very late germ-layer decisions.

Different roles for Pax6 in the optic vesicle and facial epithelium mediate early morphogenesis of the murine eye

Development ◽  
2000 ◽  
Vol 127 (5) ◽  
pp. 945-956 ◽  
Author(s):  
J.M. Collinson ◽  
R.E. Hill ◽  
J.D. West
Keyword(s):  
Histological Analysis ◽  
Eye Development ◽  
Wild Type Mouse ◽  
Lens Epithelium ◽  
Optic Vesicle ◽  
Wild Type ◽  
Adhesive Properties ◽  
Optic Vesicles ◽  
Lens Placode ◽  
Mutant Cells

Chimaeric mice were made by aggregating Pax6(−/−) and wild-type mouse embryos, in order to study the interaction between the optic vesicle and the prospective lens epithelium during early stages of eye development. Histological analysis of the distribution of homozygous mutant cells in the chimaeras showed that the cell-autonomous removal of Pax6(−/−) cells from the lens, shown previously at E12.5, is nearly complete by E9.5. Most mutant cells are eliminated from an area of facial epithelium wider than, but including, the developing lens placode. This result suggests a role for Pax6 in maintaining a region of the facial epithelium that has the tissue competence to undergo lens differentiation. Segregation of wild-type and Pax6(−/−) cells occurs in the optic vesicle at E9.5 and is most likely a result of different adhesive properties of wild-type and mutant cells. Also, proximo-distal specification of the optic vesicle (as assayed by the elimination of Pax6(−/−) cells distally), is disrupted in the presence of a high proportion of mutant cells. This suggests that Pax6 operates during the establishment of patterning along the proximo-distal axis of the vesicle. Examination of chimaeras with a high proportion of mutant cells showed that Pax6 is required in the optic vesicle for maintenance of contact with the overlying lens epithelium. This may explain why Pax6(−/−) optic vesicles are inefficient at inducing a lens placode. Contact is preferentially maintained when the lens epithelium is also wild-type. Together, these results demonstrate requirements for functional Pax6 in both the optic vesicle and surface epithelia in order to mediate the interactions between the two tissues during the earliest stages of eye development.

All-or-none craniorachischisis in Loop-tail mutant mouse chimeras

Development ◽  
1990 ◽  
Vol 110 (1) ◽  
pp. 229-237 ◽  
Author(s):  
T.S. Musci ◽  
R.J. Mullen
Keyword(s):  
Neural Tube ◽  
Mutant Gene ◽  
Mutant Phenotype ◽  
Progeny Testing ◽  
Wild Type ◽  
Glucose Phosphate ◽  
Threshold Mechanism ◽  
Mutant Cells ◽  
Intermediate Expression ◽  
Gross Examination

Mouse embryos homozygous for the mutant gene Loop-tail (Lp) are characterized by craniorachischisis, an open neural tube extending from the midbrain to the tail. In the present study, experimental chimeric mice containing mixtures of genetically mutant (from Lp/+ × Lp/+ matings) and genetically normal cells were produced. Our aim was to determine whether a ‘rescue,’ phenotypic gradient, or intermediate expression (i.e. alternating areas of open and closed neural tube) would be observed in these chimeras. We report our analyses of Loop-tail mutant chimeras (n = 82) by gross examination, progeny testing and quantitative analysis of glucose phosphate isomerase (GPI) isozyme levels. An all-or-none craniorachischisis in Loop-tail mutant chimeras was observed. Two multicolored adult chimeras, without any gross evidence of a neural tube defect, were shown to be homozygous Loop-tail chimeras (Lp/Lp in equilibrium +/+) by progeny testing. These results indicate that the normal phenotype can be expressed in the presence of mutant cells. Conversely, six neonates with craniorachischisis were shown to be chimeras by GPI analyses. These results show that the full mutant phenotype can be expressed even when one-third to one-half of the cells are genotypically wild-type. This study did not determine which tissue is primarily responsible for the defective neurulation in this mutant, but suggests that a ‘threshold’ mechanism underlies the Loop-tail mutant phenotype. In some chimeras that threshold is not reached and the neural tube remains open, whereas in other chimeras the threshold is reached and the neural tube closes completely.

Cell-autonomous shift from axial to paraxial mesodermal development in zebrafish floating head mutants

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4257-4264 ◽  
Author(s):  
M.E. Halpern ◽  
C. Thisse ◽  
R.K. Ho ◽  
B. Thisse ◽  
B. Riggleman ◽  
...  
Keyword(s):  
Neural Tube ◽  
Single Cells ◽  
Floor Plate ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Genetic Mosaics ◽  
Essential Step ◽  
Ventral Neural Tube ◽  
Mesodermal Development

Zebrafish floating head mutant embryos lack notochord and develop somitic muscle in its place. This may result from incorrect specification of the notochord domain at gastrulation, or from respecification of notochord progenitors to form muscle. In genetic mosaics, floating head acts cell autonomously. Transplanted wild-type cells differentiate into notochord in mutant hosts; however, cells from floating head mutant donors produce muscle rather than notochord in wild-type hosts. Consistent with respecification, markers of axial mesoderm are initially expressed in floating head mutant gastrulas, but expression does not persist. Axial cells also inappropriately express markers of paraxial mesoderm. Thus, single cells in the mutant midline transiently co-express genes that are normally specific to either axial or paraxial mesoderm. Since floating head mutants produce some floor plate in the ventral neural tube, midline mesoderm may also retain early signaling capabilities. Our results suggest that wild-type floating head provides an essential step in maintaining, rather than initiating, development of notochord-forming axial mesoderm.

scholarly journals The Meningococcal ABC-Type l-Glutamate Transporter GltT Is Necessary for the Development of Experimental Meningitis in Mice

2009 ◽  
Vol 77 (9) ◽  
pp. 3578-3587 ◽  
Author(s):  
Roberta Colicchio ◽  
Susanna Ricci ◽  
Florentia Lamberti ◽  
Caterina Pagliarulo ◽  
Chiara Pagliuca ◽  
...  
Keyword(s):  
Histological Analysis ◽  
Glutamate Uptake ◽  
Glutamate Transporter ◽  
Systemic Infection ◽  
Fold Increase ◽  
Wild Type ◽  
Nutrient Source ◽  
Infectious Dose ◽  
Life Threatening ◽  
The Brain

ABSTRACT Experimental animal models of bacterial meningitis are useful to study the host-pathogen interactions occurring at the cerebral level and to analyze the pathogenetic mechanisms behind this life-threatening disease. In this study, we have developed a mouse model of meningococcal meningitis based on the intracisternal inoculation of bacteria. Experiments were performed with mouse-passaged serogroup C Neisseria meningitidis. Survival and clinical parameters of infected mice and microbiological and histological analysis of the brain demonstrated the establishment of meningitis with features comparable to those of the disease in humans. When using low bacterial inocula, meningococcal replication in the brain was very efficient, with a 1,000-fold increase of viable counts in 18 h. Meningococci were also found in the blood, spleens, and livers of infected mice, and bacterial loads in different organs were dependent on the infectious dose. As glutamate uptake from the host has been implicated in meningococcal virulence, mice were infected intracisternally with an isogenic strain deficient in the ABC-type l-glutamate transporter GltT. Noticeably, the mutant was attenuated in virulence in mixed infections, indicating that wild-type bacteria outcompeted the GltT-deficient meningococci. The data show that the GltT transporter plays a role in meningitis and concomitant systemic infection, suggesting that meningococci may use l-glutamate as a nutrient source and as a precursor to synthesize the antioxidant glutathione.

The zebrafish T-box genesno tailandspadetailare required for development of trunk and tail mesoderm and medial floor plate

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3311-3323 ◽  
Author(s):  
Sharon L. Amacher ◽  
Bruce W. Draper ◽  
Brian R. Summers ◽  
Charles B. Kimmel
Keyword(s):  
Embryonic Development ◽  
Neural Tube ◽  
Transcriptional Regulators ◽  
Floor Plate ◽  
Wild Type ◽  
T Box ◽  
No Tail ◽  
Ventral Neural Tube ◽  
Plate Formation ◽  
In Cells

T-box genes encode transcriptional regulators that control many aspects of embryonic development. Here, we demonstrate that the mesodermally expressed zebrafish spadetail (spt)/VegT and no tail (ntl)/Brachyury T-box genes are semi-redundantly and cell-autonomously required for formation of all trunk and tail mesoderm. Despite the lack of posterior mesoderm in spt–;ntl– embryos, dorsal-ventral neural tube patterning is relatively normal, with the notable exception that posterior medial floor plate is completely absent. This contrasts sharply with observations in single mutants, as mutations singly in ntl or spt enhance posterior medial floor plate development. We find that ntl function is required to repress medial floor plate and promote notochord fate in cells of the wild-type notochord domain and that spt and ntl together are required non cell-autonomously for medial floor plate formation, suggesting that an inducing signal present in wild-type mesoderm is lacking in spt–;ntl– embryos.

Further studies on the melanophores of periodic albino mutant of Xenopus laevis

Development ◽  
1986 ◽  
Vol 91 (1) ◽  
pp. 65-78
Author(s):  
T. Fukuzawa ◽  
H. Ide
Keyword(s):  
Xenopus Laevis ◽  
Microscopic Level ◽  
Wild Type ◽  
Light Microscopic Level ◽  
In Vitro Proliferation ◽  
Albino Mutant ◽  
Site Of Action ◽  
Periodic Albino

It is still unknown why dermal melanophores disappear during larval development, and why no or very few epidermal melanophores appear during and after metamorphosis, in Xenopus laevis showing periodic albinism (ap). To elucidate these points, we investigated (1) the occurrence of depigmentation in mutant (ap/ap) melanophores during in vitro proliferation and (2) the incidence of melanophore differentiation from mutant melanoblasts in the skin in vitro. During in vitro proliferation of mutant melanophores, ap-type melanosomes decreased in number gradually and instead the number of premelanosomes increased in the cells, which caused depigmentation at the light microscopic level in the culture. Depigmentation was observed only in mutant melanophores, and not in wild-type (+/+) melanophores. These results suggest that autonomous depigmentation of mutant dermal melanophores is the cause of the disappearance of these cells in vivo. Dopa-positive melanoblasts were demonstrated in both wild-type and mutant skins. However, the melanoblasts of metamorphosed mutant froglets did not differentiate in vitro, while those of wild-type froglets did. These results suggest that mutant melanoblasts in the skin of froglets lose the potency to differentiate into melanophores, and that this causes the lack of mutant melanophores in the froglets. The site of action of the ap gene is also discussed.

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