scholarly journals Encore is a member of a novel family of proteins and affects multiple processes in Drosophila oogenesis

Development ◽  
2000 ◽  
Vol 127 (22) ◽  
pp. 4753-4762 ◽  
Author(s):  
C. Van Buskirk ◽  
N.C. Hawkins ◽  
T. Schupbach
Keyword(s):  
Drosophila Melanogaster ◽  
Nurse Cells ◽  
Drosophila Oogenesis ◽  
Rna Targets ◽  
Multiple Processes ◽  
Egg Chambers ◽  
Oocyte Cytoplasm ◽  
Mutant Phenotypes ◽  
Novel Protein

Mutations in the encore (enc) gene of Drosophila melanogaster cause one extra round of mitosis in the germline, resulting in the formation of egg chambers with extra nurse cells. In addition, enc mutations affect the accumulation of Gurken protein within the oocyte, leading to the production of ventralized eggs. Here we show that enc mutants also exhibit abnormalities in karyosome morphology, similar to other ventralizing mutants such as okra and spindle B. Unlike these mutants, however, the defects in Gurken accumulation and karyosome formation do not result from activation of a meiotic checkpoint. Furthermore, we demonstrate that the requirement for enc in these processes is temporally distinct from its role in germline mitosis. Cloning of the enc locus and generation of anti-Enc antibodies reveal that enc encodes a large novel protein that accumulates within the oocyte cytoplasm and colocalizes with grk mRNA. We argue that the enc mutant phenotypes reflect a role for Enc in the regulation of several RNA targets.

scholarly journals SOLO: a meiotic protein required for centromere cohesion, coorientation, and SMC1 localization in Drosophila melanogaster

2010 ◽  
Vol 188 (3) ◽  
pp. 335-349 ◽  
Author(s):  
Rihui Yan ◽  
Sharon E. Thomas ◽  
Jui-He Tsai ◽  
Yukihiro Yamada ◽  
Bruce D. McKee
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
Sister Chromatid Cohesion ◽  
Early Prophase ◽  
Wild Type ◽  
Sister Chromatids ◽  
Chromatid Cohesion ◽  
Mutant Phenotypes ◽  
Meiosis I ◽  
Novel Protein

Sister chromatid cohesion is essential to maintain stable connections between homologues and sister chromatids during meiosis and to establish correct centromere orientation patterns on the meiosis I and II spindles. However, the meiotic cohesion apparatus in Drosophila melanogaster remains largely uncharacterized. We describe a novel protein, sisters on the loose (SOLO), which is essential for meiotic cohesion in Drosophila. In solo mutants, sister centromeres separate before prometaphase I, disrupting meiosis I centromere orientation and causing nondisjunction of both homologous and sister chromatids. Centromeric foci of the cohesin protein SMC1 are absent in solo mutants at all meiotic stages. SOLO and SMC1 colocalize to meiotic centromeres from early prophase I until anaphase II in wild-type males, but both proteins disappear prematurely at anaphase I in mutants for mei-S332, which encodes the Drosophila homologue of the cohesin protector protein shugoshin. The solo mutant phenotypes and the localization patterns of SOLO and SMC1 indicate that they function together to maintain sister chromatid cohesion in Drosophila meiosis.

scholarly journals Structure and expression of hybrid dysgenesis-induced alleles of the ovarian tumor (otu) gene in Drosophila melanogaster.

Genetics ◽  
1993 ◽  
Vol 133 (2) ◽  
pp. 253-263
Author(s):  
G L Sass ◽  
J D Mohler ◽  
R C Walsh ◽  
L J Kalfayan ◽  
L L Searles
Keyword(s):  
Drosophila Melanogaster ◽  
Ovarian Tumor ◽  
P Element ◽  
Female Sterility ◽  
Protein Coding ◽  
Transcription Start Sites ◽  
Insertion And Deletion ◽  
Undifferentiated Cells ◽  
Egg Chambers ◽  
Mutant Phenotypes

Abstract Mutations at the ovarian tumor (otu) gene of Drosophila melanogaster cause female sterility and generate a range of ovarian phenotypes. Quiescent (QUI) mutants exhibit reduced germ cell proliferation; in oncogenic (ONC) mutants germ cells undergo uncontrolled proliferation generating excessive numbers of undifferentiated cells; the egg chambers of differentiated (DIF) mutants differentiate to variable degrees but fail to complete oogenesis. We have examined mutations caused by insertion and deletion of P elements at the otu gene. The P element insertion sites are upstream of the major otu transcription start sites. In deletion derivatives, the P element, regulatory regions and/or protein coding sequences have been removed. In both insertion and deletion mutants, the level of otu expression correlates directly with the severity of the phenotype: the absence of otu function produces the most severe QUI phenotype while the ONC mutants express lower levels of otu than those which are DIF. The results of this study demonstrate that the diverse mutant phenotypes of otu are the consequence of different levels of otu function.

scholarly journals Autophagic degradation of dBruce controls DNA fragmentation in nurse cells during late Drosophila melanogaster oogenesis

2010 ◽  
Vol 190 (4) ◽  
pp. 523-531 ◽  
Author(s):  
Ioannis P. Nezis ◽  
Bhupendra V. Shravage ◽  
Antonia P. Sagona ◽  
Trond Lamark ◽  
Geir Bjørkøy ◽  
...  
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Dna Fragmentation ◽  
Nurse Cell ◽  
Nurse Cells ◽  
Cell Nuclei ◽  
Cytoplasmic Material ◽  
Fragmented Dna ◽  
Egg Chambers ◽  
Autophagic Degradation

Autophagy is an evolutionarily conserved pathway responsible for degradation of cytoplasmic material via the lysosome. Although autophagy has been reported to contribute to cell death, the underlying mechanisms remain largely unknown. In this study, we show that autophagy controls DNA fragmentation during late oogenesis in Drosophila melanogaster. Inhibition of autophagy by genetically removing the function of the autophagy genes atg1, atg13, and vps34 resulted in late stage egg chambers that contained persisting nurse cell nuclei without fragmented DNA and attenuation of caspase-3 cleavage. The Drosophila inhibitor of apoptosis (IAP) dBruce was found to colocalize with the autophagic marker GFP-Atg8a and accumulated in autophagy mutants. Nurse cells lacking Atg1 or Vps34 in addition to dBruce contained persisting nurse cell nuclei with fragmented DNA. This indicates that autophagic degradation of dBruce controls DNA fragmentation in nurse cells. Our results reveal autophagic degradation of an IAP as a novel mechanism of triggering cell death and thereby provide a mechanistic link between autophagy and cell death.

Encore, a gene required for the regulation of germ line mitosis and oocyte differentiation during Drosophila oogenesis

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 281-290 ◽  
Author(s):  
N.C. Hawkins ◽  
J. Thorpe ◽  
T. Schupbach
Keyword(s):  
Germ Line ◽  
Oocyte Nucleus ◽  
Temperature Sensitive ◽  
Nurse Cells ◽  
Multiple Alleles ◽  
Drosophila Oogenesis ◽  
Isolation And Characterization ◽  
Egg Chambers ◽  
Bag Of Marbles ◽  
Oocyte Differentiation

During Drosophila oogenesis, a stem cell daughter undergoes precisely four rounds of mitosis to generate a cyst of 16 cells interconnected by cytoplasmic bridges. One of the cells becomes the oocyte while the remaining 15 cells differentiate as nurse cells. We hve identified a gene, encore, that is involved both in regulating the number of germline mitoses and in the process of oocyte differentation. Mutations in encore result in exactly one extra round of mitosis in the germline. Genetic and molecular studies indicate that this mitotic defect may be mediated through the gene bag-of-marbles. The isolation and characterization of multiple alleles of encore revealed that they were all temperature sensitive for this phenotype. Mutations in encore also affect the process of oocyte differentiation. Egg chambers are produced in which the oocyte nucleus has undergone endoreplication often resulting in the formation of 16 nurse cells. We argue that these two phenotypes produced by mutations in encore represent two independent requirements for encore during oogenesis.

The Drosophila melanogaster septin gene Sep2 has a redundant function with the retrogene Sep5 in imaginal cell proliferation but is essential for oogenesis

Genome ◽  
2013 ◽  
Vol 56 (12) ◽  
pp. 753-758 ◽  
Author(s):  
Ryan S. O’Neill ◽  
Denise V. Clark
Keyword(s):  
Cell Proliferation ◽  
Drosophila Melanogaster ◽  
Protein Level ◽  
Cytoskeletal Proteins ◽  
Biological Processes ◽  
Nurse Cells ◽  
Wild Type ◽  
Egg Chambers ◽  
And Function ◽  
Redundant Functions

Septins are cytoskeletal proteins that form hetero-oligomeric complexes and function in many biological processes, including cytokinesis. Drosophila melanogaster has five septin genes. Sep5, which is the most recently evolved septin gene in Drosophila, is a retrogene copy of Sep2. Sep5 mutants appear wild type, whereas Sep2 mutant females are semisterile. Their ovaries have egg chambers containing abnormal numbers of nurse cells. The egg chamber phenotype is rescued to wild type by expressing a Sep2 cDNA, but it is only partially rescued by expressing a Sep5 cDNA, showing that these paralogs have diverged in function at the protein level. Sep2 Sep5 double mutants have an early pupal lethal phenotype and lack imaginal discs, suggesting that these genes have redundant functions during imaginal cell proliferation.

Molecular organization and expression of the genetic locus glued in Drosophila melanogaster

1986 ◽  
Vol 6 (3) ◽  
pp. 833-841
Author(s):  
A Swaroop ◽  
J W Sun ◽  
M L Paco-Larson ◽  
A Garen
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Function ◽  
Genetic Locus ◽  
Insertion Site ◽  
Lethal Effect ◽  
P Element ◽  
Molecular Organization ◽  
General Distribution ◽  
Element Insertion ◽  
Mutant Phenotypes

The Glued locus of Drosophila melanogaster is genetically defined as the functional unit which is affected by the dominant Glued mutation Gl. Genomic DNA was cloned from the region of the Glued locus, at 70C2 on chromosome 3, by using a P element insertion in the region as a molecular marker. Three genes encoding polyadenylated transcripts were detected within a 30-kilobase span of the cloned DNA. The gene nearest the P element insertion site was identified as a Glued gene on the basis of alterations in its DNA and encoded transcript associated with the Gl mutation and with reversions of Gl which eliminate the dominant effect by inactivation of the mutant allele. Expression of the wild-type Gl+ gene is temporally regulated during development; the amount of the encoded transcript is highest in the embryonic stage, decreasing in the first and second larval instars, and then increasing in the third instar and pupal stages. There is a maternal contribution of the Gl+ transcript to the embryo, which probably accounts for the maternal lethal effect of Glued mutations on early development. In situ hybridizations of Gl+ DNA to RNA in tissue sections showed that the Gl+ transcript is present in virtually all tissues of the embryo, late larva, and pupa. The general distribution of this transcript is consistent with genetic evidence indicating that the Glued locus controls a generally essential cell function (P. J. Harte and D. R. Kankel, Genetics 101:477-501, 1982). Different Glued mutations produce distinct phenotypic effects, including adults with severe visual defects, larvae lacking imaginal discs, and early lethality. These diverse mutant phenotypes are discussed in terms of quantitative changes in the Glued function. Closely adjacent to Gl+ is another gene which is transcribed in a divergent direction and expressed coordinately with Gl+ throughout Drosophila development. It remains to be determined whether this gene is also involved with the Glued function.

Apoptosis in late stage Drosophila nurse cells does not require genes within the H99 deficiency

Development ◽  
1998 ◽  
Vol 125 (6) ◽  
pp. 1075-1082 ◽  
Author(s):  
K. Foley ◽  
L. Cooley
Keyword(s):  
Dna Fragmentation ◽  
Late Stage ◽  
Expression Patterns ◽  
Nuclear Material ◽  
Nurse Cells ◽  
Wild Type ◽  
Negative Regulators ◽  
Egg Chambers ◽  
Positive Regulators ◽  
Egg Chamber

We have determined that nurse cells are cleared from the Drosophila egg chamber by apoptosis. DNA fragmentation begins in nurse cells at stage 12, following the completion of cytoplasm transfer from the nurse cells to the oocyte. During stage 13, nurse cells increasingly contain highly fragmented DNA and disappear from the egg chamber concomitantly with the formation of apoptotic vesicles containing highly fragmented nuclear material. In dumpless mutant egg chambers that fail to complete cytoplasm transport from the nurse cells, DNA fragmentation is markedly delayed and begins during stage 13, when the majority of cytoplasm is lost from the nurse cells. These data suggest the presence of cytoplasmic factors in nurse cells that inhibit the initiation of DNA fragmentation. In addition, we have examined the ovarian expression patterns of regulatory genes implicated in Drosophila apoptosis. The positive regulators, reaper (rpr), head involution defective (hid) and grim, as well as the negative regulators, DIAP1 and DIAP2, are transcribed during oogenesis. However, germline clones homozygous for the deficiency Df(3)H99, which deletes rpr, hid and grim, undergo oogenesis in a manner morphologically indistinguishable from wild type, indicating that genes within this region are not necessary for apoptosis in nurse cells.

scholarly journals Needs and Targets for the multi sex combs Gene Product in Drosophila melanogaster

Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 1823-1838 ◽  
Author(s):  
Olivier Saget ◽  
Françoise Forquignon ◽  
Pedro Santamaria ◽  
Neel B Randsholt
Keyword(s):  
Drosophila Melanogaster ◽  
Ectopic Expression ◽  
Polycomb Group ◽  
Homeotic Genes ◽  
Maternal Control ◽  
Gap Gene ◽  
Sex Combs ◽  
Normal Expression ◽  
Selector Genes ◽  
Mutant Phenotypes

Abstract We have analyzed the requirements for the multi sex combs (mxc) gene during development to gain further insight into the mechanisms and developmental processes that depend on the important trans-regulators forming the Polycomb group (PcG) in Drosophila melanogaster. mxc is allelic with the tumor suppressor locus lethal (1) malignant blood neoplasm (l(1)mbn). We show that the mxc product is dramatically needed in most tissues because its loss leads to cell death after a few divisions. mxc has also a strong maternal effect. We find that hypomorphic mxc mutations enhance other PcG gene mutant phenotypes and cause ectopic expression of homeotic genes, confirming that PcG products are cooperatively involved in repression of selector genes outside their normal expression domains. We also demonstrate that the mxc product is needed for imaginal head specification, through regulation of the ANT-C gene Deformed. Our analysis reveals that mxc is involved in the maternal control of early zygotic gap gene expression previously reported for some PcG genes and suggests that the mechanism of this early PcG function could be different from the PcG-mediated regulation of homeotic selector genes later in development. We discuss these data in view of the numerous functions of PcG genes during development.

maelstrom is required for an early step in the establishment of Drosophila oocyte polarity: posterior localization of grk mRNA

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4661-4671 ◽  
Author(s):  
N.J. Clegg ◽  
D.M. Frost ◽  
M.K. Larkin ◽  
L. Subrahmanyan ◽  
Z. Bryant ◽  
...  
Keyword(s):  
Nurse Cell ◽  
Egf Receptor ◽  
Mrna Localization ◽  
Follicle Cells ◽  
Rna Transport ◽  
Nurse Cells ◽  
Loss Of Function ◽  
Cell Fates ◽  
Early Step ◽  
Novel Protein

We describe a mutant, maelstrom, that disrupts a previously unobserved step in mRNA localization within the early oocyte, distinct from nurse-cell-to-oocyte RNA transport. Mutations in maelstrom disturb the localization of mRNAs for Gurken (a ligand for the Drosophila Egf receptor), Oskar and Bicoid at the posterior of the developing (stage 3–6) oocyte. maelstrom mutants display phenotypes detected in gurken loss-of-function mutants: posterior follicle cells with anterior cell fates, bicoid mRNA localization at both poles of the stage 8 oocyte and ventralization of the eggshell. These data are consistent with the suggestion that early posterior localization of gurken mRNA is essential for activation of the Egf receptor pathway in posterior follicle cells. Posterior localization of mRNA in stage 3–6 oocytes could therefore be one of the earliest known steps in the establishment of oocyte polarity. The maelstrom gene encodes a novel protein that has a punctate distribution in the cytoplasm of the nurse cells and the oocyte until the protein disappears in stage 7 of oogenesis.

A maternal product of the Punch locus of Drosophila melanogaster is required for precellular blastoderm nuclear divisions

1994 ◽  
Vol 107 (12) ◽  
pp. 3501-3513 ◽  
Author(s):  
X. Chen ◽  
E.R. Reynolds ◽  
G. Ranganayakulu ◽  
J.M. O'Donnell
Keyword(s):  
Drosophila Melanogaster ◽  
Mitotic Spindles ◽  
Guanosine Triphosphate ◽  
Protein Levels ◽  
Stage Of Development ◽  
Essentially Normal ◽  
Chromosome Separation ◽  
Oocyte Cytoplasm ◽  
Mitotic Figures ◽  
Pteridine Biosynthesis

The Punch locus of Drosophila melanogaster encodes the pteridine biosynthesis enzyme guanosine triphosphate cyclohydrolase. One class of Punch mutants is defective for a maternal function that results in embryonic death. We demonstrate here that the embryos exhibit nuclear division defects during the precellular blastoderm stage of development. These defects include abnormal nuclear distribution, mitotic asynchrony, and persisting chromatin bridges. Daughter nuclei that do not complete chromosome separation nevertheless initiate new interphase and mitotic cycles. As a result, interconnected mitotic figures are observed. Mitotic spindles and nuclear envelopes appear essentially normal. A mutant phenocopy was induced in wild-type embryos by treatment with the guanosine triphosphate cyclohydrolase inhibitor, 2,4-diamino-6-hydroxypyrimidine, at a very early cleavage stage. Furthermore, an inhibitor of a terminal step in pteridine biosynthesis produced an identical phenotype. Immunolocalization experiments define expression of Punch protein in nurse cells during oogenesis. The protein is packaged into granules as it is transported into the oocyte cytoplasm. As syncytial blastoderm nuclear divisions proceed, Punch protein levels decrease and disappear by cellularization. Defects in the expression of the protein in Punch maternal effect mutants correlate well with the early phenotypes. These results show that a Punch product is directly involved in early nuclear divisions and suggest a possible role in chromosome separation.

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