Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Body Patterning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed2001

Pattern formation during C. elegans vulval induction.

Studies of C. elegans vulval development provide insights into the process of pattern formation during animal development. The invariant pattern of vulval precursor cell fates is specified by the integration of at least two signaling systems. Recent findings suggest that multiple, partially redundant mechanisms are involved in patterning the vulval precursor cells. The inductive signal activates the LET-60/RAS signaling pathway and induces the 1 degree fate, whereas the lateral signal mediated by LIN-12/Notch is required for specification of the 2 degrees fate. Several regulatory pathways antagonize the RAS signaling pathway and specify the non-vulval 3 degrees fate in the absence of induction. The temporal and spatial regulation of VPC competence and production of the inductive and the lateral signal are precisely coordinated to ensure the wild-type vulval pattern.

Animals↗
PubMed2002

Fgf8 and Fgf3 are required for zebrafish ear placode induction, maintenance and inner ear patterning.

The vertebrate inner ear develops from initially 'simple' ectodermal placode and vesicle stages into the complex three-dimensional structure which is necessary for the senses of hearing and equilibrium. Although the main morphological events in vertebrate inner ear development are known, the genetic mechanisms controlling them are scarcely understood. Previous studies have suggested that the otic placode is induced by signals from the chordamesoderm and the hindbrain, notably by fibroblast growth factors (Fgfs) and Wnt proteins. Here we study the role of Fgf8 as a bona-fide hindbrain-derived signal that acts in conjunction with Fgf3 during placode induction, maintenance and otic vesicle patterning. Acerebellar (ace) is a mutant in the fgf8 gene that results in a non-functional Fgf8 product. Homozygous mutants for acerebellar (ace) have smaller ears that typically have only one otolith, abnormal semi-circular canals, and behavioral defects. Using gene expression markers for the otic placode, we find that ace/fgf8 and Fgf-signaling are required for normal otic placode formation and maintenance. Conversely, misexpression of fgf8 or Fgf8-coated beads implanted into the vicinity of the otic placode can increase ear size and marker gene expression, although competence to respond to the induction appears restricted. Cell transplantation experiments and expression analysis suggest that Fgf8 is required in the hindbrain in the rhombomere 4-6 area to restore normal placode development in ace mutants, in close neighbourhood to the forming placode, but not in mesodermal tissues. Fgf3 and Fgf8 are expressed in hindbrain rhombomere 4 during the stages that are critical for placode induction. Joint inactivation of Fgf3 and Fgf8 by mutation or antisense-morpholino injection causes failure of placode formation and results in ear-less embryos, mimicking the phenotype we observe after pharmacological inhibition of Fgf-signaling. Fgf8 and Fgf3 together therefore act during induction and differentiation of the ear placode. In addition to the early requirement for Fgf signaling, the abnormal differentiation of inner ear structures and mechanosensory hair cells in ace mutants, pharmacological inhibition of Fgf signaling, and the expression of fgf8 and fgf3 in the otic vesicle demonstrate independent Fgf function(s) during later development of the otic vesicle and lateral line organ. We furthermore addressed a potential role of endomesomerm by studying mzoep mutant embryos that are depleted of head endomesodermal tissue, including chordamesoderm, due to a lack of Nodal-pathway signaling. In these embryos, early placode induction proceeds largely normally, but the ear placode extends abnormally to midline levels at later stages, suggesting a role for the midline in restricting placode development to dorsolateral levels. We suggest a model of zebrafish inner ear development with several discrete steps that utilize sequential Fgf signals during otic placode induction and vesicle patterning.

Acridine Orange↗
PubMed2002

Wnt signalling: refocusing on Strabismus.

Vertebrate homologues of the Strabismus/van Gogh (stbm/vang) gene have been implicated in patterning and morphogenesis during gastrulation. Recent work shows that stbm/vang is mutated in zebrafish trilobite mutants and that stbm/vang is required for morphogenesis but not patterning during zebrafish gastrulation.

Animals↗
PubMed2002

Thoughts and observations on patterning in early mammalian development.

The preimplantation mammalian conceptus shows an impressive ability to develop normally following the loss, gain or rearrangement of cells. This has prompted the view that, unlike in other species, patterning in mammals cannot depend on information that is already present in the zygote before it begins to cleave. However, various findings are hard to reconcile with this conclusion, including evidence that the incidence of monozygotic twinning is sensitive to the conditions to which eggs or very early concepti are exposed. Possible causes of early twinning are discussed, and it is argued that partial hatching of the conceptus through a hernia in the zona pellucida cannot account for all cases. Moreover, it remains questionable whether studies on aggregated morulae and isolated blastomeres really provide compelling evidence against the existence of indispensible patterning information in the egg. Finally, regularities in axial relationships between the blastocyst and zygote have been revealed employing strictly non-invasive techniques. These show that, at least in normal development, patterning begins before cleavage.

Animals↗
PubMed2003

Wingless promotes cell survival but constrains growth during Drosophila wing development.

During animal development, organs grow to a fixed size and shape. Organ development typically begins with a rapid growth phase followed by a gradual decline in growth rate as the organ matures, but the regulation of either stage of growth remains unclear. The Wnt/Wingless (Wg) proteins are critical for patterning most animal organs, have diverse effects on development and have been proposed to promote organ growth. Here we report that contrary to this view, Wg activity actually constrains wing growth during Drosophila melanogaster wing development. In addition, we demonstrate that Wg is required for wing cell survival, particularly during the rapid growth phase of wing development. We propose that the cell-survival- and growth-constraining activities of Wg function to sculpt and delimit final wing size as part of its overall patterning programme.

Animals↗
PubMed1997

Enhancement of overgrowth by gene interactions in lethal(2)giant discs imaginal discs from Drosophila melanogaster.

Recessive lethal mutations of the lethal(2)giant discs (l(2)gd) and lethal(2)fat (l(2)ft) loci of Drosophila melanogaster cause imaginal disc hyperplasia during a prolonged larval stage. Imaginal discs from l(2)ft l(2)gd or Gl(2)gd double homozygotes show more extensive overgrowth than in either single homozygote, and double homozygous l(2)ft l(2)gd mitotic clones in adult flies show much more overgrowth than is seen in clones homozygous for either l(2)gd or l(2)ft alone. dachsous (ds) also acts as an enhancer of l(2)gd, producing dramatically overgrown discs and causing failure to pupariate in double homozygotes. The comb gap (cg) mutation, which also interacts with ds, greatly enhances the tendency of imaginal discs from l(2)gd larvae to duplicate as they overgrow. If l(2)gd homozygotes are made heterozygous for l(2)ft, then several discs duplicate, indicating that l(2)ft acts an a dominant enhancer of l(2)gd. l(2)ft also acts as a dominant enhancer of l(2)gd, and conversely l(2)gd acts as a dominant modifier of l(2)ft. The enhancement of overgrowth caused by various mutant combinations is accompanied by changes in expression of Decapentaplegic and Wingless. These results show that tumor suppressor genes act in combination to control cell proliferation, and that tissue hyperplasia can be associated with ectopic expression of genes involved in pattern formation.

Animals↗
PubMed2006

Subequatorial cytoplasm plays an important role in ectoderm patterning in the sea urchin embryo.

To gain information on the process of ectoderm patterning, the animal halves of sea urchin embryos were isolated at various stages, and their morphology was examined when control embryos developed into pluteus larvae. The animal halves separated at the 8-cell stage developed into 'dauerblastula', without showing any conspicuous ectoderm differentiation. In contrast, some of the animal halves isolated at the 60-cell stage (after the sixth cleavage) formed a ciliated band and oral opening, suggesting that some patterning signal was transmitted from the vegetal to animal hemisphere during early cleavage. Further patterning of the animal hemisphere did not seem to occur until hatching, since both the animal halves isolated at the 60-cell stage and hatching stage showed the same degree of ectoderm patterning. After hatching, the later animal halves were isolated, the more patterned ectoderm they formed. The animal halves isolated just prior to gastrulation differentiated well-patterned ectoderm. It is of note, however, that the level of separation was a more crucial factor than the timing of separation; even the animal fragments of newly hatched embryos differentiated well-patterned ectoderm if they had been separated at a subequatorial level. This suggests that the signal for ectoderm patterning is transmitted over the equator after hatching, and once the cells in the supra-equatorial region receive the signal, they, in turn, can transmit the signal upwardly. Interestingly, if the third cleavage plane was shifted toward the vegetal pole, the isolated animal pole-side fragments developed into 'embryoids' with fully patterned ectoderm. These results indicate that not the micromere descendants but the subequatorial cytoplasm plays an important role in ectoderm patterning.

Animals↗
PubMed2003

Orb and a long poly(A) tail are required for efficient oskar translation at the posterior pole of the Drosophila oocyte.

During Drosophila oogenesis, the posterior determinant, Oskar, is tightly localized at the posterior pole of the oocyte. The exclusive accumulation of Oskar at this site is ensured by localization-dependent translation of oskar mRNA: translation of oskar mRNA is repressed during transport and activated upon localization at the posterior cortex. Previous studies have suggested that oskar translation is poly(A)-independent. We show that a long poly(A) tail is required for efficient oskar translation, both in vivo and in vitro, but is not sufficient to overcome BRE-mediated repression. Moreover, we show that accumulation of Oskar activity requires the Drosophila homolog of Cytoplasmic Polyadenylation Element Binding protein (CPEB), Orb. As posterior localization of oskar mRNA is an essential prerequisite for its translation, it was critical to identify an allele of orb that does localize oskar mRNA to the posterior pole of the oocyte. We show that flies bearing the weak mutation orb(mel) localize oskar transcripts with a shortened poly(A) that fails to enhance oskar translation, resulting in reduced Oskar levels and posterior patterning defects. We conclude that Orb-mediated cytoplasmic polyadenylation stimulates oskar translation to achieve the high levels of Oskar protein necessary for posterior patterning and germline differentiation.

Animals↗
PubMed2003

Xenopus Meis3 protein forms a hindbrain-inducing center by activating FGF/MAP kinase and PCP pathways.

Knockdown studies in Xenopus demonstrated that the XMeis3 gene is required for proper hindbrain formation. An explant assay was developed to distinguish between autonomous and inductive activities of XMeis3 protein. Animal cap explants caudalized by XMeis3 were recombined with explants neuralized by the BMP dominant-negative receptor protein. XMeis3-expressing cells induced convergent extension cell elongations in juxtaposed neuralized explants. Elongated explants expressed hindbrain and primary neuron markers, and anterior neural marker expression was extinguished. Cell elongation was dependent on FGF/MAP-kinase and Wnt-PCP activities. XMeis3 activates FGF/MAP-kinase signaling, which then modulates the PCP pathway. In this manner, XMeis3 protein establishes a hindbrain-inducing center that determines anteroposterior patterning in the brain.

Animals↗
PubMed2005

Specification of individual Slouch muscle progenitors in Drosophila requires sequential Wingless signaling.

The patterning of the Drosophila mesoderm requires Wingless (Wg), one of the founding members of a large family of secreted glycoproteins, the Wnt family. Little is known about how Wg provides patterning information to the mesoderm, which is neither an epithelium nor contains the site of Wg production. By studying specification of muscle founder cells as marked by the lineage-specific transcription factor Slouch, we asked how mesodermal cells interpret the steady flow of Wg. Through the manipulation of place, time and amount of Wg signaling, we have observed that Slouch founder cell cluster II is more sensitive to Wg levels than the other Slouch-positive founder cell clusters. To specify Slouch cluster I, Wg signaling is required to maintain high levels of the myogenic transcriptional regulator Twist. However, to specify cluster II, Wg not only maintains high Twist levels, but also provides a second contribution to activate Slouch expression. This dual requirement for Wg provides a paradigm for understanding how one signaling pathway can act over time to create a diverse array of patterning outcomes.

Animals↗
PubMed1999

Proximal to distal cell communication in the Drosophila leg provides a basis for an intercalary mechanism of limb patterning.

Proximodistal patterning in the Drosophila leg is elaborated from the circular arrangement of the proximal domain expressing escargot and homothorax, and the distal domain expressing Distal-less that are allocated during embryogenesis. The distal domain differentiates multiply segmented distal appendages by activating additional genes such as dachshund. Secreted signaling molecules Wingless and Decapentaplegic, expressed along the anterior-posterior compartment boundary, are required for activation of Distal-less and dachshund and repression of homothorax in the distal domain. However, whether Wingless and Decapentaplegic are sufficient for the circular pattern of gene expression is not known. Here we show that a proximal gene escargot and its activator homothorax regulate proximodistal patterning in the distal domain. Clones of cells expressing escargot or homothorax placed in the distal domain induce intercalary expression of dachshund in surrounding cells and reorient planar cell polarity of those cells. Escargot and homothorax-expressing cells also sort out from other cells in the distal domain. We suggest that inductive cell communication between the proximodistal domains, which is maintained in part by a cell-sorting mechanism, is the cellular basis for an intercalary mechanism of the proximodistal axis patterning of the limb.

Animals↗
PubMed2004

Topology and robustness in the Drosophila segment polarity network.

A complex hierarchy of genetic interactions converts a single-celled Drosophila melanogaster egg into a multicellular embryo with 14 segments. Previously, von Dassow et al. reported that a mathematical model of the genetic interactions that defined the polarity of segments (the segment polarity network) was robust (von Dassow et al. 2000). As quantitative information about the system was unavailable, parameters were sampled randomly. A surprisingly large fraction of these parameter sets allowed the model to maintain and elaborate on the segment polarity pattern. This robustness is due to the positive feedback of gene products on their own expression, which induces individual cells in a model segment to adopt different stable expression states (bistability) corresponding to different cell types in the segment polarity pattern. A positive feedback loop will only yield multiple stable states when the parameters that describe it satisfy a particular inequality. By testing which random parameter sets satisfy these inequalities, I show that bistability is necessary to form the segment polarity pattern and serves as a strong predictor of which parameter sets will succeed in forming the pattern. Although the original model was robust to parameter variation, it could not reproduce the observed effects of cell division on the pattern of gene expression. I present a modified version that incorporates recent experimental evidence and does successfully mimic the consequences of cell division. The behavior of this modified model can also be understood in terms of bistability in positive feedback of gene expression. I discuss how this topological property of networks provides robust pattern formation and how large changes in parameters can change the specific pattern produced by a network.

Animals↗
PubMed1983

[Applied physiology: the work of driving an industrial heavy-duty truck on the highway].

Scope of this work was the investigation of the following parameters: energetic metabolism, by O2 consumption measurement using the open-circuit technique; pulmonary ventilation; cardio-circulatory activity behaviour, by recording heart rate, E.C.G., arterial blood pressure and plethysmography of lower limbs; body temperature pattern; visual function, through the determination of the visual field; kidney function through urine analysis; body joints flexibility, by proper test. The subjects chosen for this investigation are three experienced heavy-duty vehicle drivers that where submitted to proper checks before, during and after having driven a 190.38 Model truck fitted with spoiler and an S.R. Viber, high cargo body tarpaulin, PTT, 43.2 tons overall weight truck, over 9 different courses including town traffic, level highway, up and downhill highway with different gradients, in a period from 9 a.m. to 8 p.m. Along the total run of 404 kilometres, covered in 364 minutes, recording of the parameters under investigation was carried out over 249 kilometres covered 240 minutes (72% of overall driving time). Energy expenditure (1.20 +/- .19 Kcal/min at rest) resulted higher on steep uphill stretches with many bends (2.28 +/- .44 Kcal/min) than on less steep up- and downhill stretches and in city traffic (1.82 +/- .21 Kcal/min). The lowest energy expenditure--in some cases lower than the value found in the experimental rest--was recorded during motorway driving (1.28 +/- .19 Kcal/min). Pulmonary ventilation was characterized by frequent changes in rate and tidal air, in strict relationship with driving work bio-mechanical requirements (operation of the steering wheel). Also heart rate underwent ariations well in line with the energy expenditure pattern: of limited magnitude in uphill driving (+33% max over the value at rest), up to values identical with those at rest in the level highway drive. No appreciable variations were recorded in the respiratory quotient, calories/ventilation ratio and oxygen pulse. No significant changes occurred in arterial blood pressure, body temperature, auditory, visual and kidney functions, and in flexibility. Conversely, slight swelling (5%) of lower limbs was noticed at the end of the driving day. It was hence proven that--from the standpoint of energy expenditure--the work performed in driving a vehicle is not too exacting and does not induce particularly high nervous stresses. However, under given conditions, such as steady speed driving in level highway, a pre-sleep state occurs in all cases approximately after the first 30 minutes of driving, which in most cases the driver is not even aware of.(ABSTRACT TRUNCATED AT 400 WORDS)

Automobile Driving↗
PubMed1988

Potentiation of 1,1-dichloroethylene hepatotoxicity: comparative effects of hyperthyroidism and fasting.

The responses of fed, fasted, and hyperthyroid (T4) Sprague-Dawley male rats to 50 mg 1,1-dichloroethylene (1,1-DCE)/kg were compared. Hyperthyroid rats received three sc injections of thyroxine (100 micrograms/100 g) at 48-hr intervals; all other rats were sham-injected. 1,1-DCE was given po in mineral oil 24 hr after the last T4 dose; controls received only mineral oil. Animals were killed at 2, 4, and 8 hr. Liver GSH contents were lowered about 55% by both fasting and T4 while GSH transferase activities were lowered about 20% by fasting and 35% by T4. Only T4 pretreatment lowered alcohol dehydrogenase activities. Liver injury (i.e., serum glutamate pyruvate transaminase, histology) after 1,1-DCE was minimal in fed rats, moderate in fasted rats, and intermediate in T4 rats. Fasted rats showed a more pronounced depletion of liver GSH after 1,1-DCE than T4 rats and only in fasted rats did the toxicant decrease activities of the detoxification enzymes. Hypoglycemia after 1,1-DCE occurred in fed rats, but more rapidly in T4 rats. In contrast, fasted rats unexpectedly became hyperglycemic after the toxicant. Patterns of body temperature change after the toxicant, which might be due to its metabolites, were dissimilar. Hypothermia was not observed in fed rats, was only transiently evident in T4 rats, but occurred rapidly within 1 hr in fasted rats and steadily became more severe. The dissimilar patterns of liver enzyme and body temperature and serum glucose change after the toxicant in the three groups are indicative of different pathways of injury potentiation by fasting and hyperthyroidism.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Limbs and tail as evolutionarily diverging duplicates of the main body axis.

Contrasting hypotheses have been proposed to explain the pervasive parallels in the patterning of arthropod and vertebrate appendages. These hypotheses either call for a common ancestor already provided with patterned appendages or body outgrowths, or for the recruitment in limb patterning of single genes or genetic cassettes originally used for purposes other than axis patterning. I suggest instead that body appendages such as arthropod and vertebrate limbs and chordate tails are evolutionarily divergent duplicates (paramorphs) of the main body axis, that is, its duplicates, albeit devoid of endodermal component. Thus, vertebrate limbs and arthropod limbs are not historical homologs, but homoplastic features only transitively related to real historical homologs. Thus, the main body axis and the axis of the appendages have distinct but not independent evolutionary histories and may be involved in processes of homeotic co-option producing effects of morphological assimilation. For instance, chordate segmentation may have originated in the posterior appendage (tail) and subsequently extended to the trunk.

Animals↗
PubMed1993

Variation in body fat distribution and breast cancer risk in the families of patients with breast cancer and control families.

BACKGROUND: The pattern of body fat distribution in women has been correlated with the risk of developing breast and endometrial cancer. The authors determined whether body fat distribution varied between first-degree relatives of patients with breast cancer and in cancer-free families by comparing the body fat distribution of first-degree relatives of patients with breast cancer with age and Quetelet Index-matched controls. METHODS: Fifty-six first-degree relatives of newly diagnosed patients with breast cancer were compared with 56 controls (non-cancer family members) matched for age and Quetelet Index and were studied for variation in body fat distribution. Anthropometric measurements were taken for the abdomen, thigh, suprailiac, subscapular, biceps, and triceps skinfold thickness; waist and hip circumference; weight; and height. The distribution of body measurements and derived ratios in both case and control family members were compared using the Student t test. RESULTS: A significant variation in body fat distribution occurred among first-degree relatives in breast cancer and control families. In families with a history of breast cancer, first-degree family members were found to have significantly greater waist:hip ratio (P < 0.001) compared with controls without family history matched for age and Quetelet Index. Other variables indicating upper body fat localization, such as abdomen and suprailiac skinfold were significantly greater in family members of patients with breast cancer compared with controls. CONCLUSIONS: A marked variation occurred in body fat localization among first-degree relatives of patients with breast cancer and in cancer-free families. This finding implies a variation in breast cancer risk in these families. Identifying family members with upper body fat distribution in breast cancer families would allow targeting of these individuals for energetic screening and risk factor reduction interventions.

Adipose Tissue↗
PubMed2006

The mouse embryo autonomously acquires anterior-posterior polarity at implantation.

The earliest recognizable sign of patterning of the mouse embryo along the anteroposterior (A-P) axis is the migration of the distal visceral endoderm (DVE) toward the future anterior side. Here we report an asymmetry in the mouse embryo at an unexpectedly early stage. The gene for Lefty1, a Nodal antagonist that influences the direction of DVE migration, was found to be asymmetrically expressed in the primitive endoderm of the implanting blastocyst. Lefty1 expression begins randomly in the inner cell mass (ICM) of the blastocyst but is regionalized to one side of the tilted ICM shortly after implantation. Asymmetric expression of Lefty1 can be established by in vitro culture, indicating that it does not require interaction with the uterus. The asymmetric Lefty1 expression is induced by Nodal signaling, although Nodal and genes for its effectors are expressed symmetrically. This asymmetry in molecular patterning of the mouse embryo pushes back the origin of the A-P body axis to the peri-implantation stage.

Animals↗
PubMed2003

Differential expression of the Drosophila BX-C in polytene chromosomes in cells of larval fat bodies: a cytological approach to identifying in vivo targets of the homeotic Ubx, Abd-A and Abd-B proteins.

We have analyzed the expression of homeotic Bithorax Complex proteins in the fat bodies of Drosophila larvae by staining with specific antibodies. We have found that these proteins are differentially expressed along the anteroposterior (AP) axis of the fat body, with patterns parallel to those previously characterized for the larval and adult epidermis. As fat body nuclei have polytene chromosomes, we were able to identify the BX-C locus and show that it assumes a strongly puffed conformation in cells actively expressing the genes of the BX-C. Immunostaining of these polytene chromosomes provided the resolution to cytologically map binding sites of the three proteins: Ubx, Abd-A and Abd-B. The results of this work provide a system with which to study the positioning of chromatin regulatory proteins in either a repressed and/or active BXC at the cytological level. In addition, the results of this work provide a map of homeotic target loci and thus constitute the basis for a systematic identification of genes that are direct in vivo targets of the BX-C genes.

Animals↗