bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrastructure of the subventricular zone in Macaca fascicularis and evidence of a mouse‐like migratory stream
Authors: Gil‐Perotin Sara , Duran‐Moreno María , Belzunegui Silvia , Luquin Maria Rosario , Garcia‐Verdugo Jose Manuel 
Published: February 2009

AbstractRecent publications have shown that the lateral wall of the lateral ventricles in the Macaca fascicularis brain, in particular the subventricular zone (SVZ), contains neural stem cells throughout adulthood that migrate through a migratory pathway (RMS) to the olfactory bulb (OB). To date, a detailed and systematic cytoarchitectural and ultrastructural study of the monkey SVZ and RMS has not been done. We found that the organization of the SVZ was similar to that of humans, with the ependymal layer surrounding the lateral ventricles, a hypocellular GAP layer formed by astrocytic and ependymal expansions, and the astrocyte ribbon, composed of astrocytic bodies. We found no cells corresponding to the type C proliferating precursor of the rodent brain. Instead, proliferating cells, expressed as Ki‐67 immunoreactivity, were predominantly young neurons concentrated in the anterior regions, and occasional astrocytes of the ribbon. We observed displaced ependymal cells of still unknown significance. New neurons tended to organize in chain‐like structures, which were surrounded by astrocytes. This pattern was highly reminiscent of that observed in rodent RMS, but not in humans. These chains spread from the frontal SVZ along a GAP‐like layer, uniquely composed of astrocytic expansions, to the olfactory bulb (OB). The number of neuronal chains and the number of chain‐forming cells decreased gradually upon reaching the OB. The purpose of this work is to provide a reference for future studies in the field of adult neurogenesis that may lead to an understanding of the fate and functionality of newborn neurons in primates, and ultimately in humans. J. Comp. Neurol. 514:533–554, 2009. © 2009 Wiley‐Liss, Inc.
Combined extrinsic and intrinsic manipulations exert complementary neuronal enrichment in embryonic rat neural precursor cultures: An in vitro and in vivo analysis
Authors: Furmanski Orion , Gajavelli Shyam , Lee Jeung Woon , Collado Maria E. , Jergova Stanislava , Sagen Jacqueline 
Published: February 2009

AbstractNumerous central nervous system (CNS) disorders share a common pathology in dysregulation of γ‐aminobutyric acid (GABA) inhibitory signaling. Transplantation of GABA‐releasing cells at the site of disinhibition holds promise for alleviating disease symptoms with fewer side effects than traditional drug therapies. We manipulated fibroblast growth factor (FGF)‐2 deprivation and mammalian achaete‐scute homolog (MASH)1 transcription factor levels in an attempt to amplify the default GABAergic neuronal fate in cultured rat embryonic neural precursor cells (NPCs) for use in transplantation studies. Naïve and MASH1 lentivirus‐transduced NPCs were maintained in FGF‐2 or deprived of FGF‐2 for varying lengths of time. Immunostaining and quantitative analysis showed that GABA‐ and β‐III‐tubulin‐immunoreactive cells generally decreased through successive passages, suggesting a loss of neurogenic potential in rat neurospheres expanded in vitro. However, FGF‐2 deprivation resulted in a small, but significantly increased population of GABAergic cells derived from passaged neurospheres. In contrast to naïve and GFP lentivirus‐transduced clones, MASH1 transduction resulted in increased bromodeoxyuridine (BrdU) incorporation and clonal colony size. Western blotting showed that MASH1 overexpression and FGF‐2 deprivation additively increased β‐III‐tubulin and decreased cyclic nucleotide phosphodiesterase (CNPase) expression, whereas FGF‐2 deprivation alone attenuated glial fibrillary acidic protein (GFAP) expression. These results suggest that low FGF‐2 signaling and MASH1 activity can operate in concert to enrich NPC cultures for a GABA neuronal phenotype. When transplanted into the adult rat spinal cord, this combination also yielded GABAergic neurons. These findings indicate that, even for successful utilization of the default GABAergic neuronal precursor fate, a combination of both extrinsic and intrinsic manipulations will likely be necessary to realize the full potential of NSC grafts in restoring function. J. Comp. Neurol. 515:56–71, 2009. © 2009 Wiley‐Liss, Inc.
Embryonic substantia nigra grafts in the mesencephalon send neurites to the host striatum in non‐human primate after overexpression of GDNF
Authors: Redmond D.E. , Elsworth J.D. , Roth R.H. , Leranth C. , Collier T.J. , Blanchard B. , Bjugstad K.B. , Samulski R.J. , Aebischer P. , Sladek J.R. 
Published: February 2009

AbstractIn spite of partial success in treating Parkinson's disease by using ectopically placed grafts of dopamine‐producing cells, restoration of the original neuroanatomical circuits, if possible, might work better. Previous evidence of normal anatomic projections from ventral mesencephalic (VM) grafts placed in the substantia nigra (SN) has been limited to neonatal rodents and double grafting or bridging procedures. This study attempted to determine whether injection of a potent growth‐promoting factor, glial cell line‐derived neurotrophic factor (GDNF), into the target regions or placement of fetal striatal co‐grafts in the nigrostriatal pathway might elicit neuritic outgrowth to the caudate nucleus. Four adult St. Kitts green monkeys received embryonic VM grafts into the rostral mesencephalon near the host SN, and injections of adeno‐associated virus 2 (AAV2)/GDNF or equine infectious anemia virus (EIAV)/GDNF into the caudate. Three adult monkeys were co‐grafted with fetal VM tissue near the SN and fetal striatal grafts (STR) 2.5 mm rostral in the nigrostriatal pathway. Before sacrifice, the striatal target regions were injected with the retrograde tracer Fluoro‐Gold (FG). FG label was found in tyrosine hydroxylase‐labeled neurons in VM grafts in the SN of only those monkeys that received AAV2/GDNF vector injections into the ipsilateral striatum. All monkeys showed FG labeling in the host SN when FG labeling was injected on the same side. These data show that grafted dopaminergic neurons can extend neurites to a distant target releasing an elevated concentration of GDNF, and suggest that grafted neurons can be placed into appropriate loci for potential tract reconstruction. J. Comp. Neurol. 515:31–40, 2009. © 2009 Wiley‐Liss, Inc.
Drosophila DHR38 nuclear receptor is required for adult cuticle integrity at eclosion
Authors: Kozlova Tatiana , Lam Geanette , Thummel Carl S. 
Published: February 2009

AbstractDHR38 is the only Drosophila member of the NR4A subclass of vertebrate nuclear receptors, which have been implicated in multiple biological pathways, including neuronal function, apoptosis, and metabolism. Although an earlier study identified three point mutations in DHR38, none of these were shown to be a null allele for the locus, leaving it unclear whether a complete loss of DHR38 function might uncover novel roles for the receptor. Here we show that a specific DHR38 null allele, DHR38Y214, leads to fully penetrant pharate adult lethality, similar to the most severe phenotype associated with the EMS‐induced mutations. DHR38Y214 mutants display minor effects on ecdysone‐regulated transcription at the onset of metamorphosis. In contrast, cuticle gene expression is significantly reduced in DHR38Y214 mutant pupae. These studies define the essential functions of DHR38 and provide a genetic context for further characterization of its roles during development. Developmental Dynamics 238:701–707, 2009. © 2009 Wiley‐Liss, Inc.
Presynaptic secretion of mind‐the‐gap organizes the synaptic extracellular matrix‐integrin interface and postsynaptic environments
Authors: Rushton Emma , Rohrbough Jeffrey , Broadie Kendal 
Published: February 2009

AbstractMind‐the‐Gap (MTG) is required during synaptogenesis of the Drosophila glutamatergic neuromuscular junction (NMJ) to organize the postsynaptic domain. Here, we generate MTG::GFP transgenic animals to demonstrate MTG is synaptically targeted, secreted, and localized to punctate domains in the synaptic extracellular matrix (ECM). Drosophila NMJs form specialized ECM carbohydrate domains, with carbohydrate moieties and integrin ECM receptors occupying overlapping territories. Presynaptically secreted MTG recruits and reorganizes secreted carbohydrates, and acts to recruit synaptic integrins and ECM glycans. Transgenic MTG::GFP expression rescues hatching, movement, and synaptogenic defects in embryonic‐lethal mtg null mutants. Targeted neuronal MTG expression rescues mutant synaptogenesis defects, and increases rescue of adult viability, supporting an essential neuronal function. These results indicate that presynaptically secreted MTG regulates the ECM‐integrin interface, and drives an inductive mechanism for the functional differentiation of the postsynaptic domain of glutamatergic synapses. We suggest that MTG pioneers a novel protein family involved in ECM‐dependent synaptic differentiation. Developmental Dynamics 238:554–571, 2009. © 2009 Wiley‐Liss, Inc.
Tendons and muscles of the mouse forelimb during embryonic development
Authors: Watson Spences S. , Riordan Timothy J. , Pryce Brian A. , Schweitzer Ronen 
Published: February 2009

AbstractThe range and precision of limb movements are dependent on the specific patterns of muscles and tendons. To facilitate analyses of tendon and muscle phenotypes we compiled a description of these tissues in the forelimb of developing mouse embryos. Individual tendons, muscles, and ligaments were annotated in a series of transverse sections through the forelimb of an embryo at day 18.5 of embryonic development (E18.5). Transverse sections present a distinctive and highly reproducible pattern of the muscles and tendons at different limb levels that can be used as a simple reference in analyses of mutant phenotypes. A comparable set of sections from an embryo at E14.5 was included to highlight structural features that change during the maturation of the musculoskeletal system. The ability to define the precise position of transverse sections along the proximal–distal axis of the limb may also be useful in studies of other features in developing limbs. Developmental Dynamics 238:693–700, 2009. © 2009 Wiley‐Liss, Inc.
FRS2α is required for the separation, migration, and survival of pharyngeal‐endoderm derived organs including thyroid, ultimobranchial body, parathyroid, and thymus
Authors: Kameda Yoko , Ito Masataka , Nishimaki Toshiyuki , Gotoh Noriko 
Published: February 2009

AbstractThe docking protein FRS2α plays an important role in fibroblast growth factor (FGF)‐induced intracellular signal transduction by linking FGF receptors (FGFRs) to a variety of intracellular signaling pathways. In FRS2α2F/2F mutant mice at embryonic day (E)18.5, in which the Shp2‐binding sites of FRS2α were disrupted, the thyroid glands were aplastic or hypoplastic. C cells were absent or present in low numbers and rarely formed a compact mass of cells. Parathyroid glands were mostly connected to thymus tissues. At E10.5, the formations of pharyngeal pouches and thyroid primordium were normally initiated in the mutant mice. At E11.5 to E12.5, the thyroid primordium of wild‐type embryos was located close to the aortic sac, and the epithelial buds of pharyngeal‐derived organs, including the parathyroid gland, thymus and ultimobranchial body, were separated from the epithelium and began to migrate to their final destinations. In the FRS2α2F/2F mutants, however, the thyroid primordium became hypoplastic and the pharyngeal‐derived organ primordia remained affiliated with the pharyngeal epithelium. At these stages, organ‐specific differentiation markers (i.e., Nkx2‐1/TTF1 for the thyroid lobe and ultimobranchial body; Pax8 for the thyroid lobe; parathormone (PTH), chromogranin A, P75NTR, and S100 protein for the parathyroid gland; and p63 for the thymus) were normally expressed in the mutant tissues. Thus, the separation, migration, and survival of the pharyngeal organs were impaired in the FRS2α2F/2F mutants. Developmental Dynamics 238:503–513, 2009. © 2009 Wiley‐Liss, Inc.
The homeobox gene Mohawk represses transcription by recruiting the sin3A/HDAC co‐repressor complex
Authors: Anderson Douglas M. , Beres Brian J. , Wilson‐Rawls Jeanne , Rawls Alan 
Published: February 2009

AbstractMohawk is an atypical homeobox gene expressed in embryonic progenitor cells of skeletal muscle, tendon, and cartilage. We demonstrate that Mohawk functions as a transcriptional repressor capable of blocking the myogenic conversion of 10T1/2 fibroblasts. The repressor activity is located in three small, evolutionarily conserved domains (MRD1–3) in the carboxy‐terminal half of the protein. Point mutation analysis revealed six residues in MRD1 are sufficient for repressor function. The carboxy‐terminal half of Mohawk is able to recruit components of the Sin3A/HDAC co‐repressor complex (Sin3A, Hdac1, and Sap18) and a subset of Polymerase II general transcription factors (Tbp, TFIIA1 and TFIIB). Furthermore, Sap18, a protein that bridges the Sin3A/HDAC complex to DNA‐bound transcription factors, is co‐immunoprecipitated by MRD1. These data predict that Mohawk can repress transcription through recruitment of the Sin3A/HDAC co‐repressor complex, and as a result, repress target genes required for the differentiation of cells to the myogenic lineage. Developmental Dynamics 238:572–580, 2009. © 2009 Wiley‐Liss, Inc.
Regulation of the Caenorhabditis elegans posterior hox gene egl‐5 by microRNA and the polycomb‐like gene sop‐2
Authors: Zhang Hongjie , Emmons Scott W. 
Published: February 2009

AbstractIn Caenorhabditis elegans, the domains of Hox gene expression are controlled by the novel global regulatory gene sop‐2. We identified a region located 3′ of the Hox gene egl‐5 that promotes ectopic expression of an egl‐5 reporter gene in a sop‐2 mutant. SOP‐2 could directly block positive regulatory factors acting in this region, or it could block their expression. We identified three possible miRNA binding sites within the egl‐5 3′ untranslated region (UTR). Cognate microRNAs are expressed in relevant tissues and can block egl‐5 expression when expressed from a transgene. Mutation of the putative binding sites in the egl‐5 3′UTR resulted in a modest degree of misexpression of a minimal egl‐5 reporter gene, suggesting that microRNAs may contribute to the tight restriction of egl‐5 expression to particular cell lineages. Developmental Dynamics 238:595–603, 2009. © 2009 Wiley‐Liss, Inc.
Recapitulation of zebrafish sncga expression pattern and labeling the habenular complex in transgenic zebrafish using green fluorescent protein reporter gene
Authors: Chen Yi‐Chung , Cheng Chia‐Hsiung , Chen Gen‐Der , Hung Chin‐Chun , Yang Chung‐Hsiang , Hwang Sheng‐Ping L. , Kawakami Koichi , Wu Bo‐Kai , Huang Chang‐Jen 
Published: February 2009

AbstractHuman synuclein family consists of α‐, β‐, and γ‐synucleins. Here, we cloned three genes, sncb, sncga and sncgb from zebrafish. They encode β‐, γ1‐, and γ2‐synucleins, respectively. The zSyn‐β, zSyn‐γ1, and zSyn‐γ2 proteins display 69%, 47%, and 50% identity to human β‐synuclein and γ‐synuclein, respectively. By reverse transcriptase‐polymerase chain reaction, we demonstrated that sncb and sncga mRNA were abundant in brain and eye, while sncgb expression was moderate in brain, kidney, ovary and testis. The 1.8‐kb 5′‐upstream/promoter region of the sncga gene was sufficient to direct green fluorescent protein (GFP) expression in the central nervous system and cranial ganglions. A transgenic line, Tg(sncga:GFP), was generated and its GFP expression is similar to that of endogenous sncga mRNA. Moreover, this line also labels the habenular complex and the domain of GFP expression is larger in the left than in the right habenula. Thus, this line can be used to study sncga gene regulation and for left–right asymmetry study in zebrafish brain. Developmental Dynamics 238:746–754, 2009. © 2009 Wiley‐Liss, Inc.
Genetic disruption of CYP26B1 severely affects development of neural crest derived head structures, but does not compromise hindbrain patterning
Authors: Maclean Glenn , Dollé Pascal , Petkovich Martin 
Published: February 2009

AbstractCyp26b1 encodes a cytochrome‐P450 enzyme that catabolizes retinoic acid (RA), a vitamin A derived signaling molecule. We have examined Cyp26b1−/− mice and report that mutants exhibit numerous abnormalities in cranial neural crest cell derived tissues. At embryonic day (E) 18.5 Cyp26b1−/− animals exhibit a truncated mandible, abnormal tooth buds, reduced ossification of calvaria, and are missing structures of the maxilla and nasal process. Some of these abnormalities may be due to defects in formation of Meckel's cartilage, which is truncated with an unfused distal region at E14.5 in mutant animals. Despite the severe malformations, we did not detect any abnormalities in rhombomere segmentation, or in patterning and migration of anterior hindbrain derived neural crest cells. Abnormal migration of neural crest cells toward the posterior branchial arches was observed, which may underlie defects in larynx and hyoid development. These data suggest different periods of sensitivity of anterior and posterior hindbrain neural crest derivatives to elevated levels of RA in the absence of CYP26B1. Developmental Dynamics 238:732–745, 2009. © 2009 Wiley‐Liss, Inc.
Cardiac cushions modulate action potential phenotype during heart development
Authors: Polo‐Parada Luis , Zhang Xiaolin , Modgi Amol 
Published: February 2009

AbstractThe extracellular matrix plays an important role in cardiac function. Its role in the generation and modulation of electrical activity in the early stages of heart development has not been studied extensively. Our study demonstrates that the extracellular matrix in cardiac cushions can alter the action potential phenotype by direct contact with cardiomyocytes from different regions of the heart. We also demonstrate that fibronectin, an important and abundant component of the cardiac extracellular matrix, partially mimics the effects of the cushion tissue in altering the changes in action potential. Fibronectin increases ICa2+ and acutely increases cytosolic calcium. These findings suggest that the composition of the cardiac extracellular matrix during development plays an important role in defining patterns of electrical activity in the developing heart. Developmental Dynamics 238:611–623, 2009. © 2009 Wiley‐Liss, Inc.
Comprehensive spatiotemporal analysis of early chick neural crest network genes
Authors: Khudyakov Jane , Bronner‐Fraser Marianne 
Published: February 2009

AbstractSpecification of neural crest progenitors begins during gastrulation at the neural plate border, long before migration or differentiation. Neural crest cell fate is acquired by progressive activation of discrete groups of transcription factors that appear to be highly conserved in vertebrates; however, comprehensive analysis of their expression has been lacking in chick, an important model system for neural crest development. To address this, we analyzed expression of 10 transcription factors that are known specifiers of neural plate border and neural crest fate and compared them across developmental stages from gastrulation to neural crest migration. Surprisingly, we find that most neural crest specifiers are expressed during gastrulation in chick, concomitant with and in similar domains as neural plate border specifiers. This finding suggests that interactions between these molecules may occur much earlier than previously thought, an important consideration for interpretation of functional studies. Developmental Dynamics 238:716–723, 2009. © 2009 Wiley‐Liss, Inc.
Fibroblast growth factor expression during skeletal fracture healing in mice
Authors: Schmid Gregory J. , Kobayashi Chikashi , Sandell Linda J. , Ornitz David M. 
Published: February 2009

AbstractFibroblast growth factors (FGFs) are important signaling molecules that regulate many stages of endochondral bone development. During the healing of a skeletal fracture, several features of endochondral bone development are reactivated. To better understand the role of FGFs in skeletal fracture healing, we quantitatively evaluated the temporal expression patterns of Fgfs, Fgf receptors (Fgfrs), and molecular markers of bone development over a 14‐day period following long bone fracture in a mouse model. These studies identify distinct groups of FGFs that are differentially expressed and suggest active stage‐specific roles for FGF signaling during the fracture repair process. Developmental Dynamics 238:766–774, 2009. © 2009 Wiley‐Liss, Inc.
Do weight and shape concerns exhibit genetic effects? Investigating discrepant findings
Authors: Spanos Alexia , Burt S. Alexandra , Klump Kelly L. 
Published: February 2009

AbstractObjective:Unlike twin studies of general weight and shape concerns, studies examining the heritability of the undue influence of weight and shape concerns on self‐evaluation have found little evidence for genetic effects. The present study sought to resolve these discrepancies by examining the heritability of both types of weight and shape concerns in a young adult twin sample.Method:Participants included 270 female twins from the Michigan State University Twin Registry. General weight and shape concerns were assessed with subscales from the Eating Disorder Examination Questionnaire (EDEQ). Similar to previous research, the undue influence of weight and shape on self‐evaluation was assessed using averaged scores from two EDEQ items.Results:The heritability of all weight and shape measures was estimated at 49–66%.Discussion:General weight and shape concerns and the undue influence of these concerns on self‐evaluation are influenced by genetic factors in young adult female twins. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010
An examination of the overlap between genetic and environmental risk factors for intentional weight loss and overeating
Authors: Wade Tracey D. , Treloar Susan A. , Heath Andrew C. , Martin Nicholas G. 
Published: February 2009

AbstractObjective:To further our understanding of how intentional weight loss (IWL) and overeating are related, we examined the shared genetic and environmental variance between lifetime IWL and overeating.Method:Interview data were available for 1,976 female twins (both members of 439 and 264 pairs of monozygotic and dizygotic twins, respectively), mean age = 40.61, SD = 4.72. We used lifetime diagnostic data for eating disorders obtained from a semistructured psychiatric telephone interview, examined in a bivariate twin analysis. Both lifetime behaviors were measured on a 3‐point scale, where absence of IWL or overeating formed one anchor on the scale and lifetime anorexia nervosa (AN) and bulimia nervosa (BN) formed the opposite anchors, respectively.Results:In line with previous findings, a higher body mass index was significantly associated with the lifetime presence of IWL and/or overeating (odds ratio = 1.13, 95% confidence interval (CI): 1.08–1.19). The best fitting twin model contained additive genetic and nonshared environmental influence influencing both IWL and overeating, with correlations between these influences of 0.61 (95% CI: 0.35–0.92) and 0.24 (95% CI: 0.07–0.42), respectively.Discussion:About 37% of genetic risk factors were considered to overlap between IWL and overeating, and with only 6% of overlap between environmental risk factors. Thus, considerable independence of risk factors was indicated. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2009