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.

scholarly journals The Drosophila engrailed and invected Genes: Partners in Regulation, Expression and Function

Genetics ◽  
1996 ◽  
Vol 142 (3) ◽  
pp. 893-906 ◽  
Author(s):  
Elizabeth Gustavson ◽  
Andrew S Goldsborough ◽  
Zehra Ali ◽  
Thomas B Kornberg
Keyword(s):  
Expression Pattern ◽  
Cultured Cells ◽  
Regulatory Region ◽  
Embryonic Lethality ◽  
Wild Type ◽  
Terminal Portion ◽  
Coding Sequence ◽  
Differential Effects ◽  
And Function ◽  
Redundant Functions

Abstract We isolated and characterized numerous engrailed and invected alleles. Among the deficiencies we isolated, a mutant lacking invected sequences was viable and phenotypically normal, a mutant lacking engrailed was an embryo lethal and had slight segmentation defects, and a mutant lacking both engrailed and invected was most severely affected. In seven engrailed alleles, mutations caused translation to terminate prematurely in the central or C-terminal portion of the coding sequence, resulting in embryonic lethality and segmentation defects. Both engrailed and invected expression declined prematurely in these mutant embryos. In wild-type embryos, engrailed and invected are juxtaposed and are expressed in essentially identical patterns. A breakpoint mutant that separates the mgrailed and invected transcription units parceled different aspects of the expression pattern to engrailed or invected. We also found that both genes cause similar defects when expressed ectopically and that the protein products of both genes act to repress transcription in cultured cells. We propose that the varied phenotypes of the engrailed alleles can be explained by the differential effects these mutants have on the combination of engrailed and invected activities, that engrailed and invected share a regulatory region, and that they encode redundant functions.

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 MYH10 governs adipocyte function and adipogenesis through its interaction with GLUT4

2021 ◽  
Author(s):  
N Kislev ◽  
L Mor-Yossef Moldovan ◽  
R Barak ◽  
M Egozi ◽  
D Benayahu
Keyword(s):  
Glucose Transporter ◽  
Cytoskeletal Proteins ◽  
Wild Type ◽  
Cytoskeletal Remodeling ◽  
Kinase C ◽  
Important Regulator ◽  
Insulin Dependent ◽  
And Function ◽  
Cellular Components ◽  
Muscle Myosin

AbstractAdipocyte differentiation is dependent on cytoskeletal remodeling processes that determine and maintain cellular shape and function. In turn, cytoskeletal proteins contribute to the filament-based network responsible for controlling adipocyte’s shape and promoting the intracellular trafficking of key cellular components. Currently, our understanding of these mechanisms remains incomplete. In this study, we identified the non-muscle myosin 10 (MYH10) as an important regulator of adipogenesis and adipocyte function through its interaction with the insulin dependent, Glucose transporter 4 (GLUT4). MYH10 depletion in preadipocytes resulted in impaired adipogenesis, with knockdown cells exhibiting disrupted morphology and reduced molecular adipogenic signals. MYH10 was shown to be in complex with GLUT4 in adipocytes, an interaction regulated by insulin induction. The missing adipogenic capacity of MYH10-KD cells was restored when they uptook GLUT4 vesicles up from neighbor wild-type cells in a co-culture system. Our results provide the first demonstration that MYH10 interacts with GLUT4 in cells and adipose tissue through the insulin pathway. The signaling cascade is regulated by the protein kinase C ζ (PKCζ), which interacts with MYH10 to modify the localization and interaction of both GLUT4 and MYH10 in adipocytes as PKCζ inhibition resulted in reduced GLUT4 and MYH10 translocation and interactions. Overall, our study establishes MYH10 as an essential regulator of GLUT4 translocation, affecting both adipogenesis and adipocyte function, highlighting its importance in future cytoskeleton-based studies in adipocytes.

Influence of the RNA content on oogenesis in the bobbed mutants of Drosophila melanogaster

Development ◽  
1971 ◽  
Vol 25 (2) ◽  
pp. 237-246
Author(s):  
Jag Mohan
Keyword(s):  
Drosophila Melanogaster ◽  
Nucleic Acid ◽  
Acid Content ◽  
Nucleic Acid Content ◽  
Wild Type ◽  
Dna And Rna ◽  
Stage Of Development ◽  
Rna Content ◽  
Egg Chambers ◽  
Total Dna

Developing egg chambers of Drosophila melanogaster (wild-type and bobbed mutants) have been examined for their nucleic acid content by cytophotometric methods. No differences were observed in the total DNA and RNA content of the egg chambers at all stages between the bobbed mutants and the wild type. It is shown that the process of oogenesis in bobbed females is prolonged, and that this prolongation occurs at all the stages of oocyte development. Since the ovaries of the bobbed females synthesize less rRNA per unit time, it is likely that this prolongation allows the egg chambers of the bobbed females to normalize their RNA content. When they achieve a given RNA content, they proceed to the next stage of development.

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.

Two missense alleles of the Drosophila melanogaster act88F actin gene are strongly antimorphic but only weakly induce synthesis of heat shock proteins

1987 ◽  
Vol 7 (9) ◽  
pp. 3084-3091
Author(s):  
C C Karlik ◽  
D L Saville ◽  
E A Fyrberg
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Flight Muscle ◽  
Structure And Function ◽  
Actin Gene ◽  
Wild Type ◽  
Diploid Complement ◽  
Flight Muscles ◽  
Shock Proteins ◽  
And Function

We have characterized two extant mutations of the flight muscle-specific act88F actin gene of Drosophila melanogaster. Both defective alleles were recovered from flightless mutants isolated previously (K. Mogami and Y. Hotta, Mol. Gen. Genet. 183:409-417, 1981). By directly sequencing the mutant alleles, we demonstrated that in act88FIfm(3)2 a single G-C to A-T transition converted arginine-28 to cysteine and that in act88FIfm(3)4 a single A-T to T-A transversion changed isoleucine-76 to phenylalanine. We showed that the actins encoded by either allele were strongly antimorphic. Mutant alleles effectively disrupted myofibril structure and function in the flight muscles of strains having the diploid complement of wild-type act88F genes. However, unlike antimorphic actins encoded by three previously characterized act88F alleles, neither that encoded by act88FIfm(3)2 nor that encoded by act88FIfm(3)4 was a strong inducer of heat shock protein synthesis.

scholarly journals MST kinases in development and disease

2015 ◽  
Vol 210 (6) ◽  
pp. 871-882 ◽  
Author(s):  
Barry J. Thompson ◽  
Erik Sahai
Keyword(s):  
Cell Proliferation ◽  
Drosophila Melanogaster ◽  
Cell Migration ◽  
Autoimmune Disease ◽  
Cell Polarity ◽  
Signaling Molecules ◽  
Organ Size ◽  
Kinase Family ◽  
And Function ◽  
Related Proteins

The mammalian MST kinase family, which is related to the Hippo kinase in Drosophila melanogaster, includes five related proteins: MST1 (also called STK4), MST2 (also called STK3), MST3 (also called STK24), MST4, and YSK1 (also called STK25 or SOK1). MST kinases are emerging as key signaling molecules that influence cell proliferation, organ size, cell migration, and cell polarity. Here we review the regulation and function of these kinases in normal physiology and pathologies, including cancer, endothelial malformations, and autoimmune disease.

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 T-β-MCA Regulates the Termination of Liver Regeneration via the P53/miR-34a/SIRT1 Positive Feedback Loop by Suppressing the FXR/SHP Signaling Pathway.

2020 ◽  
Author(s):  
Fangchao Yuan ◽  
Yao Chen ◽  
Hao Wu ◽  
Minghua Cong ◽  
Menghao Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Regeneration ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Late Phase ◽  
Liver Weight ◽  
Wild Type ◽  
Positive Feedback Loop ◽  
And Function ◽  
Shed Light

Abstract Background The capacity of the liver to restore its architecture and function assures good prognoses of patients who suffer serious hepatic injury or cancer resection. In our previous study, we initially found that the P53/miR-34a/SIRT1 positive feedback loop has a remarkable negative regulatory effect, which is related to the termination of liver regeneration. Here, we described how P53/miR-34a/SIRT1 positive feedback loop controls liver regeneration and its possible relationship with liver cancer.Method We performed partial hepatectomy (PH) in mice transfected with adenovirus (Ade) overexpressing P53 and adenovirus-associated virus (AAV) knock-downing miR-34a. LR was analyzed by liver weight/body weight, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and cell proliferation, and the related cellular signals were investigated. Bile acid (BA) levels during LR were analyzed by metabolomics of bile acids. Results We found that the P53/miR-34a/SIRT1 positive feedback loop was activated in the late phase of LR. Overexpression of P53 terminated LR early and enhanced P53/miR-34a/SIRT1 positive feedback loop expression and its proapoptotic effect. Mice from the Ade-P53 group showed smaller livers and higher levels of serum ALT and AST than control mice. While knock-down of miR-34a abolished P53/miR-34a/SIRT1 positive feedback loop during LR. Mice from anti-miR-34a group showed larger livers and lower levels of PCNA-positive cells than control mice. T-β-MCA increased gradually during LR and peaked at 7 days after PH. T-β-MCA inhibited cell proliferation and promoted cell apoptosis via facilitating the P53/miR-34a/SIRT1 positive feedback loop during LR by suppressing FXR/SHP. Conclusion The P53/miR-34a/SIRT1 positive feedback loop plays an important role in the termination of LR. Our findings shed light on the molecular and metabolic mechanisms of LR termination and provide a potential therapeutic alternative for treating P53-wild-type HCC patients.

scholarly journals The Drosophila CPEB Protein Orb Specifies Oocyte Fate by a 3′UTR-Dependent Autoregulatory Loop

Genetics ◽  
2019 ◽  
Vol 213 (4) ◽  
pp. 1431-1446 ◽  
Author(s):  
Justinn Barr ◽  
Rudolf Gilmutdinov ◽  
Linus Wang ◽  
Yulii Shidlovskii ◽  
Paul Schedl
Keyword(s):  
Single Cell ◽  
Gene Products ◽  
Messenger Rnas ◽  
Nurse Cells ◽  
Wild Type ◽  
Fate Specification ◽  
Link Type ◽  
Egg Chambers ◽  
Germline Cyst ◽  
Dependent Mechanism

orb encodes one of the two fly CPEB proteins. These widely conserved proteins bind to the 3′UTRs of target messenger RNAs (mRNAs) and activate or repress their translation. We show here that a positive autoregulatory loop driven by the orb gene propels the specification of oocyte identity in Drosophila egg chambers. Oocyte fate specification is mediated by a 3′UTR-dependent mechanism that concentrates orb mRNAs and proteins in one of the two pro-oocytes in the 16-cell germline cyst. When the orb 3′UTR is deleted, orb mRNA and protein fail to localize and all 16 cells become nurse cells. In wild type, the oocyte is specified when orb and other gene products concentrate in a single cell in region 2b of the germarium. A partially functional orb 3′UTR replacement delays oocyte specification until the egg chambers reach stage 2 of oogenesis. Before this point, orb mRNA and protein are unlocalized, as are other markers of oocyte identity, and the oocyte is not specified. After stage 2, ∼50% of the chambers successfully localize orb in a single cell, and this cell assumes oocyte identity. In the remaining chambers, the orb autoregulatory loop is not activated and no oocyte is formed. Finally, maintenance of oocyte identity requires continuous orb activity.

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