bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stage specific embryonic defects following heat shock in Drosophila
Authors: Eberlein Susan 
Published: May 2005

AbstractHeat shock of pre‐adult Drosophila disrupts development and causes phenotypic abnormalities. Type of abnormality depends on developmental stage at time of shock. Defects probably result from disruption of stage specific processes by the heat shock response (which includes reduction of normal mRNA and protein production). This study uses heat shock to study stage specific processes in early development. Short, intense shocks (2–3 min, 42–43°C) are administered to carefully staged embryos within the first 5 h of development. Stage specific defects occur following shock at syncitial blastoderm or later. Abnormal segmentation follows shock at syncitial or cellular blastoderm. Segmentation is also disrupted by shocks 1 h after the onset of gastrulation, but not by shocks at the onset of gastrulation. Segmentation defects include phenocopies of pair rule mutants, which lack parts of alternate segments. Defective shortening of the germ band is common following shock at the onset of gastrulation. Germ band shortening normally occurs several hours after the time of shock; thus heat shock specifically affects control of a later developmental process. Development does not simply cease at the time of the distrupted process; rather a specific step in the developmental sequence is omitted or altered. Stage specific defects do not occur following pre‐blastoderm shock. Pre‐blastoderm eggs have few or no normal processes controlled by transcription, and poor ability to induce the heat shock response. This suggests that stage specific defects require disruption of transcription controlled processes. Pre‐blastoderm eggs survive a 3‐min shock less well than older eggs. The ability of older eggs to induce the heat shock response probably enhances survival. The mutant hairy was also investigated. Extreme alleles show a striking pair rule phenotype, while a weak allele does not. Heat shock of animals heterozygous or homozygous for the weak allele at blastoderm specifically increases the frequency of the extreme hairy phenotype. Thus heat shock may disrupt the same developmental process as is altered by the mutation.
Differential expression of histone sequences in Drosophila following heat shock
Authors: Spadoro Joanne P. , Copertino Donald W. , Strausbaugh Linda D. 
Published: May 2005

AbstractThe expression of the sequences encoding the four nucleosomal histone proteins was examined following heat shock of a variety of Drosophila cells and was found to be highly differential. In Drosophila melanogaster KC‐O cells grown in suspension culture, there is a continuation of the synthesis of all four of the nucleosomal histone proteins following heat shock. Analysis of RNA from these cells confirms that histone messengers are transcribed and located on polysomes. This exact same pattern of histone protein synthesis occurs in KC‐O cells grown to low density on plates. In contrast, KC‐O cells grown to high density on plates exhibit a dramatic elevation of H2b protein synthesis relative to the synthesis of the other core histones. Organs from D melanogaster third instar larvae were examined to ascertain whether histone protein synthesis continues following heat shock in the organism. Different tissue types exhibited differential histone synthesis. Imaginal disks excised from heat‐shocked larvae continue to synthesize nucleosomal histones in a variable fashion. In contrast, neither fat bodies, brains, nor salivary glands continues to synthesize core histone proteins at a significant level. D hydei plated cell cultures and larval tissues fail to synthesize histones at any detectable level following a heat shock. Based on these observations, we propose that there is a differential synthesis of nucleosomal proteins in Drosophila that is highly dependent on the state of the cells prior to the heat shock.
Histochemical analysis of the ecdysterone‐regulated expression of the Drosophila genes P1 and LSP‐2
Authors: Paco‐Larson M. Luisa , Nakanishi Yoshinobu , Levine Michael , Garen Alan 
Published: May 2005

Abstract3H‐labeled DNA probes for the ecdysterone‐inducible Drosophila genes P1 and LSP‐2 were hybridized in situ to RNA in sections of embryos and larvae. Intense hybridization was detected specifically in fat body cells of third‐instar larvae and not in other cells of third‐instar larvae nor in any cells at earlier stages. These results confirm the stringent tissue‐ and stage‐specificity of P1 and LSP‐2 expression. Hybridization of both probes occurred to virtually all the cells in the fat bodies, indicating that both genes are expressed in the same cells. Since P1 expression begins several hours later than LSP‐2 expression, and appears to be induced directly by ecdysterone, this finding implies that one or more of the fat body components mediating the response to ecdysterone is gene‐specific.
Ovarian teratocarcinomas in LT/Sv mice carrying t‐mutations
Authors: Artzt Karen , Calo Catherine , Pinheiro Elizabeth Neuner , Dimeo‐Talento Althea , Tyson Frederick L. 
Published: May 2005

AbstractOvarian teratomas that result from parthenogenetic activation of oocytes provide a double tool for developmental geneties. First, they provide a way of measuring recombination between a gene and its centromere. Second, in the absence of crossing over there is the potential of producing tumors that are homozygous for genes that would be lethal in the course of in utero embryonic development. We have applied both aspects to several t‐ haplotypes containing different early acting t‐lethal genes. In a study of 26 tumors, genotyped by Southern blot analysis of the major histocompatibility complex (MHC), we measured the distance between the centromere and the start of the t‐complex as 5.6 ± 2.3 cM. We found a marked deficiency of t‐homozygous genotypes among the tumors we studied, although T/T genotypes formed teratomas at levels comparable to controls. None of the lethal t‐haplotypes we studied permit homozygous embryos to develop to the primitive streak stage, while T/T embryos do develop essentially normally through that stage. Thus, although the total number of tumors observed from t‐bearing mice was small, the great difference in the incidence of t/t tumors versus the incidence of T/T tumors suggests strongly that the parthenogeretic embryos that convert to teratocarcinomas must first pass through some of the stages of normal early development, including the formation of three germ layers and the primitive streak.
Locus determining the human sperm‐specific lactate dehydrogenase, LDHC, is syntenic with LDHC
Authors: Edwards Yvonne H. , Povey Sue , Levan Kay M. , Driscoll Catherine E. , Millan Jose Luis , Goldberg Erwin 
Published: May 2005

AbstractFrom the data presented in this report, the human LDHC gene locus is assigned to chromosome 11. Three genes determine lactate dehydrogenase (LDH) in man. LDHA and LDHB are expressed in most somatic tissues, while expression of LDHC is confined to the germinal epithelium of the testes. A human LDHC cDNA clone was used as a probe to analyze genomic DNA from rodent/human somatic cell hybrids. The pattern of bands with LDHC hybridization is easily distinguished from the pattern detected by LDHA hybridization, and the LDHC probe is specific for testis mRNA.The structural gene LDHA has been previously assigned to human chromosome 11, while LDHB maps to chromosome 12. Studies of pigeon LDH have shown tight linkage between LDHB and LDHC leading to the expectation that these genes would be syntenic in man. However, the data presented in this paper show conclusively that LDHC is syntenic with LDHA on human chromosome 11.The terminology for LDH genes LDHA, LDHB, and LDHC is equivalent to Ldhl, Ldh2, and Ldh3, respectively.
Comparative gene mapping: A valuable new tool for mammalian developmental studies
Authors: Womack James E. 
Published: May 2005

AbstractTechnological advances in the 1970s encouraged the mapping of homologous gene loci in different mammalian species, including mouse and man. One hundred eighty‐five homologous loci have now been mapped in these two species. Conservation of linkage is sufficient to identify substantial segments of the two genomes that have been left intact since their divergence from a common ancestor. The recognition of these conserved segments allows experimental manipulation of mouse chromosomes or chromosomal regions to produce models of human chromosomal anomalies of medical importance.Comparative gene mapping has been extended beyond mouse and man and the genomes of some species, including domestic cattle, appear to be more highly conserved relative to humans than the mouse. Such species may be particularly useful in providing models of human chromosomal anomalies that cannot be duplicated in laboratory mice.
DNA methylation in plants
Authors: Hepburn Angus G. , Belanger Faith C. , Mattheis James R. 
Published: May 2005

AbstractHigher plant DNA is extensively methylated, but the two methylated sequences (CpG and CpNpG) show different characteristics. Using sequence analysis techniques, we demonstrate that while CpG methylation follows the existing models for cytosine methylation in animals, CpNpG methylation does not. Although there is evidence to support the suggestion that the low CpG frequency has arisen from deaminational conversion of 5‐methylcytosine to thymidine, there appears to be no comparable conversion of 5‐methylcytosine in the CpNpG configuration. It therefore appears that between the evolution of CpG and CpNpG cytosine methylation systems, a mechanism evolved for the correction of C→T conversion, probably using the methylated strand to direct the repair in the correct direction.
G‐proteins in the signal‐transduction pathways of Dictyostelium discoideum
Authors: Ewa Snaar‐Jagalska B. , Kesbeke Fanja , Van Haastert Peter J. M. 
Published: May 2005

AbstractThe functional interaction of surface cAMP receptors with effector enzymes via G‐proteins was investigated in Dictyostelium discoideum. Several experimental conditions were used to investigate signal transduction, such as reduced temperatures, use of down‐regulated cells and of mutants. The results are presented as a model describing the complex interaction between multiple forms of the surface cAMP receptor and different G‐proteins that are responsible for the generation of the second messengers, cAMP, cGMP, InsP3 and Ca2+.
Glycogen phosphorylase in Dictyostelium discoideum: Demonstration of two developmentally regulated forms, purification to homogeneity, immunochemical analysis, cAMP induction, in vitro translation, and molecular cloning
Authors: Rutherford C. L. , Naranan V. , Brickey D. A. , Sucic J. F. , Rogers P. V. , Selmin O. 
Published: May 2005

AbstractA key step in the cellular differentiation of Dictyostelium is the degradation of glycogen to provide the precursors for synthesis of the structural end products of development. We have found that the enzyme that initiates this degradative pathway, glycogen phosphorylase (1,4‐α‐D‐glucan:orthophosphate α‐glucosyltransferase; EC 2.4.1.1), is developmentally regulated and exists as two forms. During the time course of development, a previously undescribed activity, the “b” form, decreases, while that of the “a” form increases. The “b” form is inactive unless 5′AMP is included in the reaction mixture. The two forms differ in their elution from DE52 cellulose, affinity constants, thermal stability, affinity for 5′AMP Sepharose, subunit molecular weight, and peptide maps. In crude extracts, anti‐a antiserum stains a 104‐kD protein that is associated with phosphorylase “a” activity and appears late in development, while anti‐b antiserum stains a 92‐kD protein that is associated with phosphorylase “b” activity and is present throughout development. We have also demonstrated in vitro phosphorylation of the “b” form by an endogenous protein kinase and a corresponding loss of 5′AMP dependence. If intact cells were exposed to exogenous cAMP, “b” activity decreased and was replaced by “a” activity, as well as the 104‐kD protein band on SDS‐PAGE. In order to determine if the two forms of the enzyme are different gene products, we screened lambda gt11 expression libraries with antibodies against the purified “a” and “b” forms. Three clones were found to be overlapping by Southern analysis. A yeast glycogen phosphorylase cDNA clone (gpy) and a human muscle glycogen phosphorylase clone (HM‐11) cross‐hybridized with the Dictyostelium inserts, and gpy shared a few common restriction fragments with the Dictyostelium clones on genomic blots. Northern analysis of Dictyostelium total RNA showed that the Dictyostelium inserts and gpy recognize an mRNA of 3.2 kb, while on poly A‐enriched RNA, the yeast clone detects preferentially a 3.6‐kb message.
Stalk cell formation in monolayers of Dictyostelium discoideum V12‐M2
Authors: Sobolewski Andre , Kwong Linda , Weeks Gerald 
Published: May 2005

AbstractStalk cell formation in low‐cell‐density monolayers of Dictyostelium discoideum, strain V12‐M2, occurs following the sequential addition of cyclic AMP and the differentiation‐inducing factor (DIF). Both cyclic AMP and DIF are essential for the appearance of the prestalk‐specific isozyme alkaline phosphatase‐II, which suggests that both factors are necessary for prestalk cell formation. The available evidence suggests that the cyclic AMP requirement for stalk cell formation is mediated through the cell surface cyclic AMP receptor. However, stalk cell formation is inhibited by caffeine and this inhibition is reversed by the cell‐permeable analogue 8‐Br‐cyclic AMP, which suggests in addition a possible involvement for elevated intracellular cyclic AMP concentrations in stalk cell formation.During in vivo development ceils first become independent of cyclic AMP at the tipped aggregate stage, but the acquisition of cyclic AMP independence is advanced by several hours when cells are incubated in the presence of cyclic AMP for 2 hours. Cells do not become independent of DIF until the culmination stage of development, which suggests the possibility that DIF is required for the conversion of prestalk cells to stalk cells.There is an absolute requirement for DIF for stalk cell formation in low‐density monolayers of prestalk cells but only part of population exhibits a requirement for cyclic AMP, which suggests that the prestalk cell population consists of two distinct cell types. Stalk cell formation from prespore cells is totally dependent on both cyclic AMP and DIF.When isolated prestalk and prespore cells are plated in high‐density monolayers, the former cells accumulate more DIF. which suggests the possibility that DIF is preferentially synthesized by prestalk cells.
A comparison of high frequency switching in the yeast Candida albicans and the slime mold Dictyostelium discoideum
Authors: Soll David R. , Kraft Bernard 
Published: May 2005

AbstractRecently, high frequency switching systems have been identified in the infectious yeast Candida albicans and the cellular slime mold Dictyostelium discoideum. In C. albicans, cells can switch at spontaneous frequencies as high as 10−2 between seven general colony morphologies in the case of strain 3153A or between two major phenotypes in the white‐opaque transition in strain WO‐1. In the latter system, dramatic changes occur in cellular phenotype as well. In D. discoideum, cells can switch at spontaneous frequencies of roughly 10−2 between a number of colony phenotypes which include alterations in developmental timing, blocks at particular morphogenetic stages, morphological aberrations, and aggregation‐minus. In the C. albicans and D. discoideum switching systems, the following characteristics are shared: (l) a limited number of switch phenotypes; (2) heritability; (3) high frequency reversibility; (4) low and high frequency modes of switching; and (5) ultraviolet (UV) stimulation of switching of cells in a low frequency mode of switching.
Organization and developmental timing of the Bombyx mori chorion gene clusters in strain C108
Authors: Goldsmith Marian R. 
Published: May 2005

AbstractWe have standardized the map of chorion structural gene clusters in Bombyx mori strain C108 by analyzing quantitative and qualitative chorion electrophoretic markers in recombinant progeny from four independent crosses. In all we assigned 22 markers to three gene clusters, representing about one‐third of the total number of chorion genes: 2 to Ch 1, 9 to Ch 2, and 8 to Ch 3. Three additional markers belong either to Ch 7 or Ch 2. By referring to published chorion protein synthesis patterns, we show that the clusters are restricted in their developmental specificities: Ch 3 appears to be an early locus, carrying all of the mapped early markers (4) and half of the early middles (3/6), while Ch 1 and Ch 2 carry predominantly middle (4/5) and all late, Hc (6) markers, along with some early middle markers (3). We cite evidence to show that Ch 1 and Ch 2 compose the left and right halves of a single gene cluster, which we formally designate as Ch 1–2.
Use of promoter fusions in Drosophila genetics: Characterization of a YP1‐ADH fusion gene
Authors: Aprison Barry S. , Osterbur David L. , Bonner J. Jose 
Published: May 2005

AbstractIn Drosophila melanogaster the yolk protein (YP) genes are normally expressed only in the fat body and follicular epithelium of adult females‐never in males or in larvae. We describe here a first step toward a genetic examination of the developmental controls that restrict the activity of the YP genes to adult female tissues. A YP1 promoter that contains the tissue‐, temporal‐, and sex‐specific controlling elements for expression was fused to the reporter gene, alcohol dehy‐drogenase (Adh). The gene fusion was transformed into an Adh‐deficient genotype. As assayed by a number of criteria, that the fusion gene is expressed in the same physiological manner as the endogenous yolk protein genes. The fusion gene's activity is modulated in trans by a temperature‐sensitive allele of the sex determination gene, tra‐2. The Adh enzyme serves as a selectable marker and therefore these flies are suitable for use in genetic screens for trons‐acting mutations that affect the expression of the yolk protein genes.
Set of proteins shows abnormal posttranslational modification in embryos homozygous for dominant T‐mutations
Authors: Park C.‐H. Thomas , Artzt Karen , Bennett Dorothea 
Published: May 2005

AbstractT and Tc are dominant mutations in the mouse that affect neuroaxial development when heterozygous and cause embryonic death when homozygous. Embryos were analyzed individually by two‐dimensional gel electrophoresis at 9½ days gestation, 1 day before homozygotes die in utero. A comparison of the protein patterns of mutant homozygotes with those of their littermates revealed a set of proteins (T‐proteins) that showed isoelectric point (pl) polymorphism. All the T‐proteins were more basic in mutant homozygotes. These polymorphisms could be detected, although they were less pronounced, in embryos as young as 7½‐day presomite stages, when it is impossible to distinguish homozygous mutants grossly. Interestingly, the same proteins show a pl shift from basic to acidic in wild‐type embryos during development from 7½ to 9½ days. Thus, it appears that in T and Tc mutants a developmentally specific posttranslational acidic modification of these proteins is disturbed. The likely cause of the abnormality is a defect in some mechanism for phosphorylation, since the T‐proteins of wild‐type embryos were shifted to higher pls by phosphatase treatment. This disturbance appears to be localized to axial structures (neural tube, somites, and surrounding mesenchyme) since only these structures, and not the rest of the mutant homozygous embryos, contain abnormally basic T‐proteins.
Dominant flightless phenotype of the vestigial‐Depilate deficiency of Drosophila melanogaster
Authors: Cripps Richard M. , Sparrow John C. 
Published: May 2005

AbstractThis paper describes the flightless phenotype of the vestigial‐Depilate deficiency of Drosophila melanogaster. Recombination experiments and studies of revertants show that the dominant flightless and depilate phenotypes are inseparable from the deficiency and due to a single cause. Dosage studies on this region reveal that these phenotypes are due to antimorphic effects, probably on the Suppressor‐2 of zeste or Posteriorsexcomb genes which lie close to the distal breakpoint of the deficiency. The deficiency does not uncover a gene haplo‐insufficient for flight. A detailed phenotypic examination failed to reveal any effects of this mutation on the indirect flight muscles. Dr(2R)vgD/+ heterozygotes are unable to initiate flight or raise their wings, even during death by over etherisation. There is a close correlation between the dominant antimorphic flightlessness and patterned thoracic bristle loss which is revealed in interactions with Df(2R)vg62 and the Su(z)2alleles. This is discussed in the light of the bnstle loss mutants of the Achaete‐scute complex. It is proposed that the vestigial‐Depilate deficiency affects the development of thoracic nerves.
Stage‐specific gene expression in early chick embryo
Authors: Zagris Nikolas , Matthopoulos Demetrios 
Published: May 2005

AbstractInhibition of DNA replication by aphidicolin in the chick morula interferes with its progression to a normal blastula and prevents induction of the first morphogenetic cell movements of primitive streak formation. Embryos in aphidicolin synthesize some polypeptides typical of blastula but do not display all the characteristic features of morula to blastula transition. Inhibition of DNA replication inteferes with the sequential synthesis of maternally coded polypeptides and with the activation of the embryonic genome in the chick embryo.
Expression of a methotrexate resistant dihydrofolate reductase gene in transgenic mice
Authors: Isola Luis M. , Gordon Jon W. 
Published: May 2005

AbstractWe have previously demonstrated systemic resistance to methotrexate (MTX) in transgenic mice carrying a foreign, mutant dihydrofolate reductase (DHFR, E.C. 1.5.1.3) gene. The new gene was introduced as a cDNA cloned into an expression vector driven by the simian virus 40 (SV40) early promoter. Previous physiologic studies suggested that transgenic mice tolerated drug doses invariably lethal to controls on the basis of gastrointestinal (GI) resistance to MTX. In the present study we evaluated foreign gene expression at the RNA level in the three major sites of MTX toxicity: intestine, liver, and bone marrow.The transgene was transcriptionally active in small bowel, and levels of expression were high in animals tolerating the largest doses of MTX. The gene was also expressed in the liver in some pedigrees, but was not detected in hemopoietic tissues of any of the pedigrees tested. Our studies correlate the site of expression of a drug resistant dhfr gene with an altered physiologic response to MTX, and demonstrate that transgenic mice can be used as a test system for expression of genes considered for use in somatic gene therapy.