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1.
BMJ Open ; 14(8): e081201, 2024 Aug 24.
Article in English | MEDLINE | ID: mdl-39181563

ABSTRACT

PURPOSE: We developed a comprehensive sleeve gastrectomy (SG) weight loss study cohort and biorepository to uncover mechanisms, biomarkers and predictive factors of weight loss, weight maintenance and amelioration of obesity-related comorbidities. For this purpose, we collected psychosocial, anthropometric, clinical data and a variety of samples pre-surgery, intraoperatively and 1.5, 3, 12 and 24 months post-surgery. For longer-term assessment, the collection of psychosocial and anthropometric data was extended to 10 years. Here, we present in-depth characterisation of the cohort and detailed overview of study procedures as a foundation for future analyses. PARTICIPANTS: We consented 647 participants between June 2017 and March 2020 from two bariatric surgery clinics in New York City-one major urban hospital and one private hospital. Of 355 participants who provided baseline data, 300 underwent SG. Of these, 79% are females with an average age of 38 years, 68% are Hispanic, 20% are non-Hispanic Black and 11% are non-Hispanic White. FINDINGS TO DATE: We collected intraoperative adipose and stomach tissues from 282 patients and biosamples (blood, urine, saliva, stool) from 245 patients at 1.5 months, 238 at 3 month, 218 at 12 months and 180 at 24 months post-surgery. We are currently collecting anthropometric and psychosocial data annually until 10 years post-surgery. Data analysis is currently underway. FUTURE PLANS: Our future research will explore the variability in weight loss outcomes observed in our cohort, particularly among Black and Hispanic patients in comparison to their White counterparts. We will identify social determinants of health, metabolic factors and other variables that may predict weight loss success, weight maintenance and remission of obesity-related comorbidities. Additionally, we plan to leverage our biorepository for collaborative research studies. We will complete long-term follow-up data by December 2031. We plan to apply for funding to expand biosample collection through year 10 to provide insights into the mechanisms of long-term weight maintenance.


Subject(s)
Gastrectomy , Obesity, Morbid , Weight Loss , Humans , Female , Adult , Gastrectomy/methods , Male , Obesity, Morbid/surgery , Longitudinal Studies , Middle Aged , Bariatric Surgery/methods , United States , Research Design , Cohort Studies
2.
J Pain ; : 104625, 2024 Jul 11.
Article in English | MEDLINE | ID: mdl-39002743

ABSTRACT

Widespread pain (WP) is associated with reduced function and disability. Importantly, three-fourths of the approximately 42% of U.S. adults with obesity have WP. Moreover, rates of adult obesity are higher, and WP outcomes are worse in racialized non-Hispanic Black and Hispanic/Latino/a/X groups, potentially exacerbating existing pain disparities. Bariatric surgery significantly reduces weight and improves pain. However, recurrent or unresolved pain after bariatric surgery can hinder weight loss or facilitate weight regain. The current study conducted a secondary analysis of a longitudinal study of predictors and mechanisms of weight loss after bariatric surgery to examine the point prevalence of WP and pain trajectories 24 months post surgery. Our secondary aim was to examine the association between weight loss and pain characteristics. Our exploratory aim was to longitudinally examine racial differences in pain trajectories after bariatric surgery. Our results showed that point prevalence decreased after bariatric surgery. Additionally, significant improvements in pain trajectories occurred within the first 3 months post surgery with a pattern of pain reemergence beginning at 12 months post surgery. Hispanic/Latino/a/X participants reported a higher number of painful anatomical sites before bariatric surgery, and the rate of change in this domain for this group was faster compared with the racialized non-Hispanic Black participants. These findings suggest that pain improvements are most evident during the early stages of surgical weight loss in racialized populations of adults with WP. Thus, clinicians should routinely monitor patients' weight changes after bariatric surgery as they are likely to correspond to changes in their pain experiences. PERSPECTIVE: This article presents the prevalence and pain trajectories of racialized adults with WP after surgical weight loss. Clinicians should evaluate changes in the magnitude and spatial distribution of pain after significant weight change in these populations so that pain interventions can be prescribed with greater precision.

3.
Pediatr Obes ; 17(3): e12856, 2022 03.
Article in English | MEDLINE | ID: mdl-34581027

ABSTRACT

BACKGROUND: Limited research has addressed the obesity-COVID-19 severity association in paediatric patients. OBJECTIVE: To determine whether obesity is an independent risk factor for COVID-19 severity in paediatric patients and whether age modifies this association. METHODS: SARS-CoV-2-positive patients at NYU Langone Health from 1 March 2020 to 3 January 2021 aged 0-21 years with available anthropometric measurements: weight, length/height and/or body mass index (BMI). Modified log-Poisson models were utilized for the analysis. Main outcomes were 1) hospitalization and 2) critical illness (intensive care unit [ICU] admission). RESULTS: One hundred and fifteen of four hundred and ninety-four (23.3%) patients had obesity. Obesity was an independent risk factor for critical illness (adjusted risk ratio [ARR] 2.02, 95% CI 1.17 to 3.48). This association was modified by age, with obesity related to a greater risk for critical illness in adolescents (13-21 years) [ARR 3.09, 95% CI 1.48 to 6.47], but not in children (0-12 years). Obesity was not an independent risk factor for hospitalization for any age. CONCLUSION: Obesity was an independent risk factor for critical illness in paediatric patients, and this association was modified by age, with obesity related to a greater risk for critical illness in adolescents, but not in children. These findings are crucial for patient risk stratification and care.


Subject(s)
COVID-19 , Adolescent , Adult , Body Mass Index , Child , Child, Preschool , Hospitalization , Humans , Infant , Infant, Newborn , Obesity/complications , Obesity/epidemiology , Risk Factors , SARS-CoV-2 , Severity of Illness Index , Young Adult
5.
PLoS One ; 14(4): e0215571, 2019.
Article in English | MEDLINE | ID: mdl-31009509

ABSTRACT

BACKGROUND: Because of the strong link between childhood obesity and adulthood obesity comorbidities, and the difficulty in decreasing body mass index (BMI) later in life, effective strategies are needed to address this condition in early childhood. The ability to predict obesity before age five could be a useful tool, allowing prevention strategies to focus on high risk children. The few existing prediction models for obesity in childhood have primarily employed data from longitudinal cohort studies, relying on difficult to collect data that are not readily available to all practitioners. Instead, we utilized real-world unaugmented electronic health record (EHR) data from the first two years of life to predict obesity status at age five, an approach not yet taken in pediatric obesity research. METHODS AND FINDINGS: We trained a variety of machine learning algorithms to perform both binary classification and regression. Following previous studies demonstrating different obesity determinants for boys and girls, we similarly developed separate models for both groups. In each of the separate models for boys and girls we found that weight for length z-score, BMI between 19 and 24 months, and the last BMI measure recorded before age two were the most important features for prediction. The best performing models were able to predict obesity with an Area Under the Receiver Operator Characteristic Curve (AUC) of 81.7% for girls and 76.1% for boys. CONCLUSIONS: We were able to predict obesity at age five using EHR data with an AUC comparable to cohort-based studies, reducing the need for investment in additional data collection. Our results suggest that machine learning approaches for predicting future childhood obesity using EHR data could improve the ability of clinicians and researchers to drive future policy, intervention design, and the decision-making process in a clinical setting.


Subject(s)
Body Mass Index , Machine Learning , Pediatric Obesity/physiopathology , Adolescent , Adult , Child , Child, Preschool , Electronic Health Records/statistics & numerical data , Female , Humans , Logistic Models , Longitudinal Studies , Male , Pediatric Obesity/diagnosis , Prognosis , ROC Curve , Retrospective Studies , Risk Factors
6.
Biochim Biophys Acta ; 1838(2): 546-56, 2014 Feb.
Article in English | MEDLINE | ID: mdl-23680625

ABSTRACT

T cells constitute a crucial arm of the adaptive immune system and their optimal function is required for a healthy immune response. After the initial step of T cell-receptor (TCR) triggering by antigenic peptide complexes on antigen presenting cell (APC), the T cell exhibits extensive cytoskeletal remodeling. This cytoskeletal remodeling leads to the formation of an "immunological synapse" [1] characterized by regulated clustering, segregation and movement of receptors at the interface. Synapse formation regulates T cell activation and response to antigenic peptides and proceeds via feedback between actin cytoskeleton and TCR signaling. Actin polymerization participates in various events during the synapse formation, maturation, and eventually its disassembly. There is increasing knowledge about the actin effectors that couple TCR activation to actin rearrangements [2,3], and how defects in these effectors translate into impairment of T cell activation. In this review we aim to summarize and integrate parts of what is currently known about this feedback process. In addition, in light of recent advancements in our understanding of TCR triggering and translocation at the synapse, we speculate on the organizational and functional diversity of microfilament architecture in the T cell. This article is part of a Special Issue entitled: Reciprocal influences between cell cytoskeleton and membrane channels, receptors and transporters. Guest Editor: Jean Claude Hervé.


Subject(s)
Actin Cytoskeleton/metabolism , Cell Communication , Receptors, Antigen, T-Cell/metabolism , Animals , Humans , Signal Transduction
7.
Curr Top Membr ; 72: 313-46, 2013.
Article in English | MEDLINE | ID: mdl-24210434

ABSTRACT

The immunological synapse (IS) is an excellent example of cell-cell communication, where signals are exchanged between two cells, resulting in a well-structured line of defense during adaptive immune response. This process has been the focus of several studies that aimed at understanding its formation and subsequent events and has led to the realization that it relies on a well-orchestrated molecular program that only occurs when specific requirements are met. The development of more precise and controllable T cell activation systems has led to new insights including the role of mechanotransduction in the process of formation of the IS and T cell activation. Continuous advances in our understanding of the IS formation, particularly in the context of T cell activation and differentiation, as well the development of new T cell activation systems are being applied to the establishment and improvement of immune therapeutical approaches.


Subject(s)
Cell Membrane/metabolism , Immunological Synapses/metabolism , Animals , Cell Communication , Cell Differentiation , Cell Membrane/immunology , Immunological Synapses/immunology , Immunotherapy , Leukemia, Myeloid/immunology , Leukemia, Myeloid/metabolism , Leukemia, Myeloid/therapy , Mechanotransduction, Cellular , Receptors, Antigen, T-Cell/metabolism , Signal Transduction , T-Lymphocytes/cytology , T-Lymphocytes/immunology , T-Lymphocytes/metabolism , Vertebrates/metabolism
8.
Nano Lett ; 13(11): 5619-26, 2013.
Article in English | MEDLINE | ID: mdl-24117051

ABSTRACT

Antigen recognition is a key event during T cell activation. Here, we introduce nanopatterned antigen arrays that mimic the antigen presenting cell surface during T cell activation. The assessment of activation related events revealed the requirement of a minimal density of 90-140 stimulating major histocompatibility complex class II proteins (pMHC) molecules per µm(2). We demonstrate that these substrates induce T cell responses in a pMHC dose-dependent manner and that the number of presented pMHCs dominates over local pMHC density.


Subject(s)
Antigen-Presenting Cells/immunology , Lymphocyte Activation/immunology , Nanoparticles/chemistry , T-Lymphocytes/immunology , Antigen-Presenting Cells/chemistry , Humans , Major Histocompatibility Complex/immunology , Membrane Proteins/immunology , Synapses/immunology , T-Lymphocytes/chemistry
9.
Front Immunol ; 3: 230, 2012.
Article in English | MEDLINE | ID: mdl-22912631

ABSTRACT

The role of non-muscle myosin IIA (heavy chain encoded by the non-muscle myosin heavy chain 9 gene, Myh9) in immunological synapse formation is controversial. We have addressed the role of myosin IIA heavy chain protein (MYH9) in mouse T cells responding to MHC-peptide complexes and ICAM-1 in supported planar bilayers - a model for immunological synapse maturation. We found that reduction of MYH9 expression levels using Myh9 siRNA in proliferating mouse CD4(+) AND T cell receptor (TCR) transgenic T cells resulted in increased spreading area, failure to assemble the central and peripheral supramolecular activation clusters (cSMAC and pSMAC), and increased motility. Surprisingly, TCR microcluster speed was reduced marginally, however TCR microclusters dissipated prior to forming a cSMAC. TCR microclusters formed in the Myh9 siRNA-treated T cells showed reduced phosphorylation of the Src family kinase (SFK) activation loop and displayed reduced cytoplasmic calcium ion (Ca(2+)) elevation. In addition, Myh9 siRNA-treated cells displayed reduced phosphorylation of the Cas-L substrate domain - a force-dependent SFK substrate - which was observed in control siRNA-treated cells in foci throughout the immunological synapse except the cSMAC. Cas-L exhibited TCR ligation-dependent induction of phosphorylation. These results provide further evidence that T cell activation is modulated by intrinsic force-generating systems and can be viewed as a mechanically responsive process influenced by MYH9.

10.
Curr Biol ; 20(20): 1840-5, 2010 Oct 26.
Article in English | MEDLINE | ID: mdl-20933420

ABSTRACT

Transport of chloride through the cystic fibrosis transmembrane conductance regulator (CFTR) channel is a key step in regulating fluid secretion in vertebrates [1, 2]. Loss of CFTR function leads to cystic fibrosis [1, 3, 4], a disease that affects the lungs, pancreas, liver, intestine, and vas deferens. Conversely, uncontrolled activation of the channel leads to increased fluid secretion and plays a major role in several diseases and conditions including cholera [5, 6] and other secretory diarrheas [7] as well as polycystic kidney disease [8-10]. Understanding how CFTR activity is regulated in vivo has been limited by the lack of a genetic model. Here, we used a forward genetic approach in zebrafish to uncover CFTR regulators. We report the identification, isolation, and characterization of a mutation in the zebrafish cse1l gene that leads to the sudden and dramatic expansion of the gut tube. We show that this phenotype results from a rapid accumulation of fluid due to the uncontrolled activation of the CFTR channel. Analyses in zebrafish larvae and mammalian cells indicate that Cse1l is a negative regulator of CFTR-dependent fluid secretion. This work demonstrates the importance of fluid homeostasis in development and establishes the zebrafish as a much-needed model system to study CFTR regulation in vivo.


Subject(s)
Body Fluids/metabolism , Cellular Apoptosis Susceptibility Protein/metabolism , Cystic Fibrosis Transmembrane Conductance Regulator/metabolism , Gastrointestinal Tract/metabolism , Homeostasis/physiology , Zebrafish Proteins/metabolism , Animals , Cell Line , Dogs , Gastrointestinal Tract/abnormalities , Gastrointestinal Tract/embryology , Genes, Recessive , Green Fluorescent Proteins , Immunoprecipitation , Microscopy, Confocal , Mutation/genetics , Zebrafish
11.
Semin Liver Dis ; 30(3): 288-95, 2010 Aug.
Article in English | MEDLINE | ID: mdl-20665380

ABSTRACT

Liver regeneration has traditionally been investigated in mammalian models. Recent technological developments in mouse genetics have greatly enhanced the resolving power of these studies. In addition, the zebrafish system has emerged as a complementary genetic system to study liver regeneration. One of the most promising attributes of the zebrafish system is its amenability to large-scale screens including genetic and chemical screens. Also, as our understanding of liver development is becoming more detailed, it is important to evaluate the commonalities and differences between organ development and regeneration.


Subject(s)
Liver Diseases/physiopathology , Liver Regeneration , Liver/physiopathology , Animals , Cell Proliferation , Cell Transdifferentiation , Hepatectomy , Humans , Liver/metabolism , Liver/pathology , Liver/surgery , Liver Diseases/metabolism , Liver Diseases/pathology , Liver Diseases/therapy , Mice , Models, Animal , Signal Transduction , Zebrafish
12.
Dis Model Mech ; 3(7-8): 486-95, 2010.
Article in English | MEDLINE | ID: mdl-20483998

ABSTRACT

Understanding liver development should lead to greater insights into liver diseases and improve therapeutic strategies. In a forward genetic screen for genes regulating liver development in zebrafish, we identified a mutant--oliver--that exhibits liver-specific defects. In oliver mutants, the liver is specified, bile ducts form and hepatocytes differentiate. However, the hepatocytes die shortly after their differentiation, and thus the resulting mutant liver consists mainly of biliary tissue. We identified a mutation in the gene encoding translocase of the outer mitochondrial membrane 22 (Tomm22) as responsible for this phenotype. Mutations in tomm genes have been associated with mitochondrial dysfunction, but most studies on the effect of defective mitochondrial protein translocation have been carried out in cultured cells or unicellular organisms. Therefore, the tomm22 mutant represents an important vertebrate genetic model to study mitochondrial biology and hepatic mitochondrial diseases. We further found that the temporary knockdown of Tomm22 levels by morpholino antisense oligonucleotides causes a specific hepatocyte degeneration phenotype that is reversible: new hepatocytes repopulate the liver as Tomm22 recovers to wild-type levels. The specificity and reversibility of hepatocyte ablation after temporary knockdown of Tomm22 provides an additional model to study liver regeneration, under conditions where most hepatocytes have died. We used this regeneration model to analyze the signaling commonalities between hepatocyte development and regeneration.


Subject(s)
Genes, Mitochondrial , Hepatocytes/cytology , Liver Regeneration/genetics , Membrane Transport Proteins/genetics , Mitochondrial Proteins/genetics , Models, Animal , Zebrafish Proteins/genetics , Zebrafish/genetics , Zebrafish/metabolism , Animals , Apoptosis/drug effects , Cell Survival/drug effects , Cell Survival/genetics , Endoderm/cytology , Endoderm/drug effects , Endoderm/metabolism , Gene Knockdown Techniques , Hepatocytes/drug effects , Hepatocytes/metabolism , Liver Regeneration/drug effects , Membrane Transport Proteins/metabolism , Mitochondrial Membrane Transport Proteins , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Mitochondrial Precursor Protein Import Complex Proteins , Mitochondrial Proteins/metabolism , Mutant Proteins/metabolism , Mutation/genetics , Oligonucleotides, Antisense/pharmacology , Organ Specificity/drug effects , Phenotype , Protein Transport/drug effects , Protein Transport/genetics , Signal Transduction/drug effects , Wnt Proteins/metabolism , Yeasts/drug effects , Yeasts/metabolism , Zebrafish Proteins/metabolism
13.
Development ; 136(1): 95-105, 2009 Jan.
Article in English | MEDLINE | ID: mdl-19036801

ABSTRACT

During Drosophila oogenesis, Oskar mRNA is transported to the posterior pole of the oocyte, where it is locally translated and induces germ-plasm assembly. Oskar protein recruits all of the components necessary for the establishment of posterior embryonic structures and of the germline. Tight localization of Oskar is essential, as its ectopic expression causes severe patterning defects. Here, we show that the Drosophila homolog of mammalian Lasp1 protein, an actin-binding protein previously implicated in cell migration in vertebrate cell culture, contributes to the accumulation of Oskar protein at the posterior pole of the embryo. The reduced number of primordial germ cells in embryos derived from lasp mutant females can be rescued only with a form of Lasp that is capable of interacting with Oskar, revealing the physiological importance of the Lasp-Oskar interaction.


Subject(s)
Actins/metabolism , Body Patterning , Drosophila Proteins/metabolism , Drosophila melanogaster/embryology , Drosophila melanogaster/metabolism , Embryo, Nonmammalian/metabolism , Microfilament Proteins/metabolism , Animals , Drosophila Proteins/chemistry , Drosophila melanogaster/cytology , Embryo, Nonmammalian/cytology , Microfilament Proteins/chemistry , Mutation/genetics , Oocytes/cytology , Oocytes/metabolism , Phenotype , Protein Binding , Protein Transport , src Homology Domains
14.
Nat Protoc ; 3(6): 948-54, 2008.
Article in English | MEDLINE | ID: mdl-18536643

ABSTRACT

Ablation studies are used to elucidate cell lineage relationships, developmental roles for specific cells during embryogenesis and mechanisms of tissue regeneration. Previous chemical and genetic approaches to directed cell ablation have been hampered by poor specificity, limited efficacy, irreversibility, hypersensitivity to promoter leakiness, restriction to proliferating cells, slow inducibility or complex genetics. Here, we provide a step-by-step protocol for a hybrid chemical-genetic cell ablation method in zebrafish that, by combining spatial and temporal control, is cell-type specific, inducible, reversible, rapid and scaleable. Bacterial Nitroreductase (NTR) is used to catalyze the reduction of the innocuous prodrug metrodinazole (Mtz), thereby producing a cytotoxic product that induces cell death. Based on this principle, NTR is expressed in transgenic zebrafish using a tissue-specific promoter. Subsequent exposure to Mtz by adding it to the media induces cell death exclusively within NTR(+) cells. This approach can be applied to regeneration studies, as removing Mtz by washing permits tissue recovery. Using this protocol, cell ablation can be achieved in 12-72 h, depending on the transgenic line used, and recovery initiates within the following 24 h.


Subject(s)
Nitroreductases/metabolism , Zebrafish/growth & development , Zebrafish/physiology , Animals , Animals, Genetically Modified , Cell Death/drug effects , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Metronidazole/metabolism , Metronidazole/toxicity , Microscopy, Fluorescence , Nitroreductases/genetics , Oxidation-Reduction , Prodrugs/metabolism , Recombinant Fusion Proteins/genetics , Recombinant Fusion Proteins/metabolism , Zebrafish/genetics
15.
Dev Dyn ; 236(4): 1025-35, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17326133

ABSTRACT

Conditional targeted cell ablation in zebrafish would greatly expand the utility of this genetic model system in developmental and regeneration studies, given its extensive regenerative capabilities. Here, we show that, by combining chemical and genetic tools, one can ablate cells in a temporal- and spatial-specific manner in zebrafish larvae. For this purpose, we used the bacterial Nitroreductase (NTR) enzyme to convert the prodrug Metronidazole (Mtz) into a cytotoxic DNA cross-linking agent. To investigate the efficiency of this system, we targeted three different cell lineages in the heart, pancreas, and liver. Expression of the fusion protein Cyan Fluorescent Protein-NTR (CFP-NTR) under control of tissue-specific promoters allowed us to induce the death of cardiomyocytes, pancreatic beta-cells, and hepatocytes at specific times. Moreover, we have observed that Mtz can be efficiently washed away and that, upon Mtz withdrawal, the profoundly affected tissue can quickly recover. These findings show that the NTR/Mtz system is effective for temporally and spatially controlled cell ablation in zebrafish, thereby constituting a most promising genetic tool to analyze tissue interactions as well as the mechanisms underlying regeneration.


Subject(s)
Genes, Transgenic, Suicide , Genetic Engineering/methods , Regeneration/physiology , Zebrafish/physiology , Animals , Animals, Genetically Modified , Embryo, Nonmammalian , Gene Expression Regulation, Developmental , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Heart/physiology , Hepatocytes/physiology , Insulin-Secreting Cells/physiology , Models, Biological , Myocardium/cytology , Myocytes, Cardiac/cytology , Nitroreductases/genetics , Nitroreductases/metabolism , Organ Specificity/genetics , Phenotype , Promoter Regions, Genetic , Zebrafish/embryology , Zebrafish/genetics
16.
Cell ; 127(3): 462-4, 2006 Nov 03.
Article in English | MEDLINE | ID: mdl-17081969

ABSTRACT

Fish and amphibian hearts are known to regenerate after partial resection, but the molecular mechanisms underlying this process remain unclear. In this issue of Cell, Lipilina et al. analyze regeneration in the zebrafish heart. Their work indicates that new cardiomyocytes originate from undifferentiated progenitor cells and reveals a critical role for the epicardium, the cellular layer that covers the heart.


Subject(s)
Heart/physiology , Pericardium/injuries , Regeneration/physiology , Stem Cells/physiology , Zebrafish/physiology , Animals , Animals, Genetically Modified , Animals, Outbred Strains , Cell Differentiation , Heart Injuries/pathology , Heart Injuries/physiopathology , Heart Ventricles/pathology , Heart Ventricles/physiopathology , Male , Models, Cardiovascular , Myocardium/metabolism , Myocardium/pathology , Regeneration/genetics , Zebrafish/genetics
17.
PLoS Genet ; 1(4): e55, 2005 Oct.
Article in English | MEDLINE | ID: mdl-16254604

ABSTRACT

This article reports the production of an EP-element insertion library with more than 3,700 unique target sites within the Drosophila melanogaster genome and its use to systematically identify genes that affect embryonic muscle pattern formation. We designed a UAS/GAL4 system to drive GAL4-responsive expression of the EP-targeted genes in developing apodeme cells to which migrating myotubes finally attach and in an intrasegmental pattern of cells that serve myotubes as a migration substrate on their way towards the apodemes. The results suggest that misexpression of more than 1.5% of the Drosophila genes can interfere with proper myotube guidance and/or muscle attachment. In addition to factors already known to participate in these processes, we identified a number of enzymes that participate in the synthesis or modification of protein carbohydrate side chains and in Ubiquitin modifications and/or the Ubiquitin-dependent degradation of proteins, suggesting that these processes are relevant for muscle pattern formation.


Subject(s)
Drosophila Proteins/genetics , Drosophila melanogaster/genetics , Gene Expression Regulation, Developmental , Genetic Techniques , Muscles/metabolism , Animals , Body Patterning , Cell Cycle , Cell Movement , Cytoskeleton/metabolism , Genes, Insect , Muscle Fibers, Skeletal/metabolism , Muscles/cytology , Muscles/pathology , Ubiquitin/metabolism
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