Bristle patterns and compartment boundaries in the tarsi of Drosophila

Development ◽  
1979 ◽  
Vol 51 (1) ◽  
pp. 195-208
Author(s):  
Peter A. Lawrence ◽  
Gary Struhl ◽  
Gines Morata

We describe cell lineage of the tarsus of wild-type Drosophila. Large Minute+ clones were made to map the position of the antero-posterior compartment boundary in all three tarsi. The tarsus is mirror symmetric, but the compartment boundary does not coincide with the mirror plane. This boundary runs along the dorsal and the ventral rows of bristles which are immediately posterior to the mirror plane; elements in these rows being made by both anterior and posterior polyclones. The provenance of bristles and bracts suggests that the bristle cells move into their final positions. The homoeotic mutation engrailed affects only the posterior compartments of all three tarsi. The mutations bithorax and postbithorax affect only the anterior and posterior compartments of the third legs, respectively, transforming them into homologous compartments of the second leg. These results support the selector gene model of development (Garcia-Bellido, 1975) and emphasize that collaboration between polyclones is important in pattern formation.

Development ◽  
1982 ◽  
Vol 68 (1) ◽  
pp. 37-57 ◽  
Author(s):  
D. Gubb ◽  
A. García-Bellido

The polarity mutants pk, sple, mwh, fz and in alter the orientations of cuticular processes in several regions of the body. The mutant polarity patterns are constant and do not result from alterations in cell lineage. Polarity patterns are locus specific rather than allele specific (new alleles express the same polarity patterns as the original alleles). In the wing, polarity formation is largely cell autonomous and is independent of the anteroposterior compartment boundary. By genetic and physiological manipulation it is shown that the mutant polarity patterns are unaffected by the size of the wing blade or the number of cells that form it. Mutants which remove parts of the wing margin or alter the distribution pattern of wing veins do not alter the mutant polarity patterns. Thus, neither the wing margins nor the pattern of vein tissue act as spatial references for polarity formation. The determination of mutant polarity patterns is not dependent on the overall topology of the wing blade but is region-specific. The mutants affect several independent functions. The possible wild-type function of the loci in polarity formation is discussed.


2018 ◽  
Vol 98 (1) ◽  
pp. 98-106 ◽  
Author(s):  
J. Kim ◽  
Y. Ahn ◽  
D. Adasooriya ◽  
E.J. Woo ◽  
H.J. Kim ◽  
...  

Crown shapes in mammalian teeth vary considerably from species to species, and morphological characters in crown shape have been used to identify species. Cusp pattern is one of the characters in crown shape. In the processes governing the formation of cusp pattern, the Shh pathway has been implicated as an important player. Suppression of Shh signaling activity in vitro in explant assays appears to induce supernumerary cusp formation in wild-type tooth germs. However, the in vivo role of Shh signaling in cusp pattern formation and the molecular mechanisms by which Shh regulates cusp patterning are not clear. Here, through in vivo phenotypic analyses of mice in which Shh activity was suppressed and compared with wild-type mice, we characterized differences in the location, number, incidence, and shape of supernumerary cusps in molars at embryonic day 15.5. We found that the distances between cusps were reduced in molars of Shh activity–suppressed mice in vivo. These findings confirm and extend the previous idea that Shh acts as an inhibitor in the reaction-diffusion model for cusp pattern formation by negatively regulating the intercuspal distance. We uncovered a significant reduction of expression level of Sostdc1, which encodes a secreted modulator of Wnt signaling, after suppression of Shh activity. The supernumerary cusp formation in Sostdc1−/− mice and compound Sostdc1 and Lrp mutant mice indicates a strong association between Wnt and Shh signaling pathways in cusp patterning. In further support of this idea, there is a high degree of similarity in the supernumerary cusp patterns of mice lacking Sostdc1 or Shh at embryonic day 15.5. These results suggest that Shh plays an inhibitory role in cusp pattern formation by modulating Wnt signaling through the positive regulation of Sostdc1.


Genetics ◽  
1972 ◽  
Vol 70 (4) ◽  
pp. 595-610
Author(s):  
Ray Moree

ABSTRACT The viability effects of chromosomes from an old and from a new laboratory strain of D. melanogaster were studied in eight factorial combinations and at two heterozygosity levels. The combinations were so constructed that heterozygosity level could be varied in the third chromosomes of the carriers of a homozygous lethal marker, in the third chromosomes of their wild-type segregants, and in the genetic backgrounds of both. Excluding the effect of the marker and the exceptional outcomes of two of the combinations, and taking into account both large and small deviations from theoretical expectation, the following summary is given as the simplest consistent explanation of the results: 1) If total heterozygosities of two segregant types tend toward equality their viabilities tend toward equality also, whether background heterozygosity is high or low; if background heterozygosities is higher the tendency toward equality is slightly greater. 2) If total heterozygosity of two segregant types are unequal the less heterozygous type has the lower viability; the difference is more pronounced when background heterozygosity is low, less when it is high. 3) Differences between segregant viabilities are correlated with differences between the total heterozygosities of the two segregants; genetic background is effective to the extent, and only to the extent, that it contributes to the magnitude of this difference. This in turn appears to underlie, at least partly, the expression of a pronounced interchromosomal epistasis. Thus in this study viability is seen to depend upon both the quantity and distribution of heterozygosity, not only among the chromosomes of an individual but among the individuals of a given combination as well.


Development ◽  
1999 ◽  
Vol 126 (23) ◽  
pp. 5295-5307 ◽  
Author(s):  
G. Weidinger ◽  
U. Wolke ◽  
M. Koprunner ◽  
M. Klinger ◽  
E. Raz

In many organisms, the primordial germ cells have to migrate from the position where they are specified towards the developing gonad where they generate gametes. Extensive studies of the migration of primordial germ cells in Drosophila, mouse, chick and Xenopus have identified somatic tissues important for this process and demonstrated a role for specific molecules in directing the cells towards their target. In zebrafish, a unique situation is found in that the primordial germ cells, as marked by expression of vasa mRNA, are specified in random positions relative to the future embryonic axis. Hence, the migrating cells have to navigate towards their destination from various starting positions that differ among individual embryos. Here, we present a detailed description of the migration of the primordial germ cells during the first 24 hours of wild-type zebrafish embryonic development. We define six distinct steps of migration bringing the primordial germ cells from their random positions before gastrulation to form two cell clusters on either side of the midline by the end of the first day of development. To obtain information on the origin of the positional cues provided to the germ cells by somatic tissues during their migration, we analyzed the migration pattern in mutants, including spadetail, swirl, chordino, floating head, cloche, knypek and no isthmus. In mutants with defects in axial structures, paraxial mesoderm or dorsoventral patterning, we find that certain steps of the migration process are specifically affected. We show that the paraxial mesoderm is important for providing proper anteroposterior information to the migrating primordial germ cells and that these cells can respond to changes in the global dorsoventral coordinates. In certain mutants, we observe accumulation of ectopic cells in different regions of the embryo. These ectopic cells can retain both morphological and molecular characteristics of primordial germ cells, suggesting that, in zebrafish at the early stages tested, the vasa-expressing cells are committed to the germ cell lineage.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (5) ◽  
pp. 774-775 ◽  
Author(s):  

This statement describes a modification of the recommended routine schedule for administering trivalent oral poliomyelitis vaccine (OPV). The American Academy of Pediatrics previously has recommended that healthy children receive a three-dose primary series of OPV at 2, 4, and 15 to 18 months of age and a fourth dose at the time of school entry (4 to 6 years of age).1 Available data indicate that the response rates to the third dose of OPV administered at 6 months of age are as good as the rates following administration of this dose at 15 to 18 months of age. Completion of the three-dose primary series at an earlier age will help health care providers induce immunity against poliomyelitis at an early age. Although wild type poliomyelitis has not caused disease in the United States for many years, the virus remains prevalent in many countries. Continued introduction of the virus into the United States by travelers could result in transmission and disease if high levels of immunity are not maintained in preschool age children. For example, wild type poliovirus type 3 was recently introduced into Canada by a religious sect that did not believe in immunization.2 The virus was probably imported from the Netherlands, where a small epidemic of poliomyelitis occurred in members of the same sect in 1992 and 1993.3 SERUM ANTIBODY RESPONSE FOLLOWING OPV ADMINISTRATION After two doses of OPV are administered at 2 and 4 months of age, 89 to 100% of children vaccinated in the United States have evidence of humoral immunity to poliomyelitis types 1 and 3, and 99 to 100% have immunity to type 2 (Table).


Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1203-1212 ◽  
Author(s):  
Katerina Nestoras ◽  
Helena Lee ◽  
Jym Mohler

We have undertaken a genetic analysis of new strong alleles of knot (kn). The original kn1 mutation causes an alteration of wing patterning similar to that associated with mutations of fused (fu), an apparent fusion of veins 3 and 4 in the wing. However, unlike fu, strong kn mutations do not affect embryonic segmentation and indicate that kn is not a component of a general Hh (Hedgehog)-signaling pathway. Instead we find that kn has a specific role in those cells of the wing imaginal disc that are subject to ptc-mediated Hh-signaling. Our results suggest a model for patterning the medial portion of the Drosophila wing, whereby the separation of veins 3 and 4 is maintained by kn activation in the intervening region in response to Hh-signaling across the adjacent anterior-posterior compartment boundary.


Development ◽  
2002 ◽  
Vol 129 (4) ◽  
pp. 973-982 ◽  
Author(s):  
Sarah Childs ◽  
Jau-Nian Chen ◽  
Deborah M. Garrity ◽  
Mark C. Fishman

Little is known about how vascular patterns are generated in the embryo. The vasculature of the zebrafish trunk has an extremely regular pattern. One intersegmental vessel (ISV) sprouts from the aorta, runs between each pair of somites, and connects to the dorsal longitudinal anastomotic vessel (DLAV). We now define the cellular origins, migratory paths and cell fates that generate these metameric vessels of the trunk. Additionally, by a genetic screen we define one gene, out of bounds (obd), that constrains this angiogenic growth to a specific path. We have performed lineage analysis, using laser activation of a caged dye and mosaic construction to determine the origin of cells that constitute the ISV. Individual angioblasts destined for the ISVs arise from the lateral posterior mesoderm (LPM), and migrate to the dorsal aorta, from where they migrate between somites to their final position in the ISVs and dorsal longitudinal anastomotic vessel (DLAV). Cells of each ISV leave the aorta only between the ventral regions of two adjacent somites, and migrate dorsally to assume one of three ISV cell fates. Most dorsal is a T-shaped cell, based in the DLAV and branching ventrally; the second constitutes a connecting cell; and the third an inverted T-shaped cell, based in the aorta and branching dorsally. The ISV remains between somites during its ventral course, but changes to run mid-somite dorsally. This suggests that the pattern of ISV growth ventrally and dorsally is guided by different cues. We have also performed an ENU mutagenesis screen of 750 mutagenized genomes and identified one mutation, obd that disrupts this pattern. In obd mutant embryos, ISVs sprout precociously at abnormal sites and migrate anomalously in the vicinity of ventral somite. The dorsal extent of the ISV is less perturbed. Precocious sprouting can be inhibited in a VEGF morphant, but the anomalous site of origin of obd ISVs remains. In mosaic embryos, obd somite causes adjacent wild-type endothelial cells to assume the anomalous ISV pattern of obd embryos. Thus, the launching position of the new sprout and its initial trajectory are directed by inhibitory signals from ventral somites. Zebrafish ISVs are a tractable system for defining the origins and fates of vessels, and for dissecting elements that govern patterns of vessel growth.


Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 149-162 ◽  
Author(s):  
U. Mayer ◽  
G. Buttner ◽  
G. Jurgens

gnom is one of several genes that make substantial contributions to pattern formation along the apical-basal axis of polarity in the Arabidopsis embryo as indicated by the mutant seedling phenotype. The apical and basal end regions of the body pattern, which include the meristems of the shoot and the root, fail to form, and a minority of mutant embryos lack morphological features of apical-basal polarity. We have investigated the developmental basis of the gnom mutant phenotype, taking advantage of a large number of EMS-induced mutant alleles. The seedling phenotype has been traced back to the early embryo in which the asymmetric division of the zygote is altered, now producing two nearly equal-sized cells. The apical daughter cell then undergoes abnormal divisions, resulting in an octant embryo with about twice the normal number of cells while the uppermost derivative of the basal cell fails to become the hypophysis, which normally contributes to root development. Consistent with this early effect, gnom appears to be epistatic to monopteros in doubly mutant embryos, suggesting that, without prior gnom activity, the monopteros gene cannot promote root and hypocotyl development. On the other hand, when root formation was induced in bisected seedlings, wild-type responded whereas gnom mutants failed to produce a root but formed callus instead. These results suggest that gnom activity promotes asymmetric cell division which we believe is necessary both for apical-basal pattern formation in the early embryo and for root formation in tissue culture.


2019 ◽  
Vol 53 (1) ◽  
pp. 505-530 ◽  
Author(s):  
Larissa B. Patterson ◽  
David M. Parichy

Vertebrate pigment patterns are diverse and fascinating adult traits that allow animals to recognize conspecifics, attract mates, and avoid predators. Pigment patterns in fish are among the most amenable traits for studying the cellular basis of adult form, as the cells that produce diverse patterns are readily visible in the skin during development. The genetic basis of pigment pattern development has been most studied in the zebrafish, Danio rerio. Zebrafish adults have alternating dark and light horizontal stripes, resulting from the precise arrangement of three main classes of pigment cells: black melanophores, yellow xanthophores, and iridescent iridophores. The coordination of adult pigment cell lineage specification and differentiation with specific cellular interactions and morphogenetic behaviors is necessary for stripe development. Besides providing a nice example of pattern formation responsible for an adult trait of zebrafish, stripe-forming mechanisms also provide a conceptual framework for posing testable hypotheses about pattern diversification more broadly. Here, we summarize what is known about lineages and molecular interactions required for pattern formation in zebrafish, we review some of what is known about pattern diversification in Danio, and we speculate on how patterns in more distant teleosts may have evolved to produce a stunningly diverse array of patterns in nature.


2002 ◽  
Vol 48 (9) ◽  
pp. 1406-1411 ◽  
Author(s):  
Jess G Evans ◽  
Cindy Lee-Tataseo

Abstract Background: Methods for analysis of the single-nucleotide polymorphism (SNP) known as factor V Leiden (FVL) are described. The technique provides rapid, highly accurate detection of the point mutation that encodes for replacement of arginine-506 with glutamine. After formal assay qualification, 758 clinical samples that had previously been analyzed by the InvaderTM Monoplex Assay were tested as research samples in a commercial clinical laboratory. Methods: Primers specific for factor V (FV) were prepared, and PCR was performed. Samples were analyzed using the NanoChip® Molecular Biology Workstation with fluorescently labeled reporters for wild-type and SNP sequences. Results: Of the 635 samples classified by the Third WaveTM assay as FV wild type, 10 were identified as heterozygous FVL by the NanoChip technique. Similarly, of the 114 putative heterozygous samples, 4 were wild type, and of the 9 reported homozygous samples, 6 were homozygous, 2 were heterozygous, and 1 was FV wild type by the NanoChip assay. All 17 results that were discordant with the Third Wave analysis were confirmed by DNA sequencing to be correctly classified by the NanoChip technology. The Nanochip system was 100% accurate in characterizing wild-type, heterozygous, and homozygous samples compared with accuracies of 99.2%, 90.2%, and 100% for the comparable Third Wave analysis. Conclusions: The NanoChip microelectronic chip array technology is an accurate and convenient method for FVL screening of research samples in a clinical laboratory environment.


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