scholarly journals Mouse oocytes develop in cysts with the help of nurse cells

2021 ◽  
Author(s):  
Wanbao Niu ◽  
Allan C Spradling
Keyword(s):  
Cell Death ◽  
Germ Cells ◽  
Nurse Cell ◽  
Cell Selection ◽  
Nurse Cells ◽  
Cell Turnover ◽  
Cell Nuclei ◽  
Body Formation ◽  
Mouse Oocytes ◽  
Cytoplasmic Transfer

Mammalian oocytes develop initially in cysts containing many more germ cells than the primordial oocytes they generate. We identified abundant nurse cells with reduced unique molecular identifiers (UMI)/cell from ovaries aged E14.5 to P1. Low UMI nurse cells are found in cysts and express the same major meiotic genes as pro-oocytes of the same stage, suggesting they are oocyte sisters that are signaled to transfer cytoplasm at different times and only subsequently diverge. Oocyte vs nurse cell selection occurs in cysts with a robust microtubule cytoskeleton, that closely interact with somatic cells and that develop a dense actin cytoskeleton around nurse cell nuclei that are held back from cytoplasmic transfer. Mouse and Drosophila nurse cells undergo programmed cell death by acidification from adjacent somatic pre-granulosa cells that express V-ATPases and cathepsin proteins. Disrupting acidification in cultured mouse ovaries blocked nurse cell turnover. About 200 genes are induced in mouse dictyate oocytes as previously reported, including Tuba1c and Tubb2b, genes that we find contribute to Balbiani body formation. Thus, mouse oocytes are specified within germline cysts and develop with the assistance of nurse cells using highly conserved mechanisms.

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.

scholarly journals Vps13 is required for timely removal of nurse cell corpses

Development ◽  
2020 ◽  
Vol 147 (20) ◽  
pp. dev191759
Author(s):  
Anita I. E. Faber ◽  
Marianne van der Zwaag ◽  
Hein Schepers ◽  
Ellie Eggens-Meijer ◽  
Bart Kanon ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Programmed Cell Death ◽  
Nurse Cell ◽  
Close Association ◽  
Follicle Cells ◽  
Nurse Cells ◽  
Lipid Transfer ◽  
Membranous Structure ◽  
Membrane Contact Sites

ABSTRACTProgrammed cell death and consecutive removal of cellular remnants is essential for development. During late stages of Drosophila melanogaster oogenesis, the small somatic follicle cells that surround the large nurse cells promote non-apoptotic nurse cell death, subsequently engulf them, and contribute to the timely removal of nurse cell corpses. Here, we identify a role for Vps13 in the timely removal of nurse cell corpses downstream of developmental programmed cell death. Vps13 is an evolutionarily conserved peripheral membrane protein associated with membrane contact sites and lipid transfer. It is expressed in late nurse cells, and persistent nurse cell remnants are observed when Vps13 is depleted from nurse cells but not from follicle cells. Microscopic analysis revealed enrichment of Vps13 in close proximity to the plasma membrane and the endoplasmic reticulum in nurse cells undergoing degradation. Ultrastructural analysis uncovered the presence of an underlying Vps13-dependent membranous structure in close association with the plasma membrane. The newly identified structure and function suggests the presence of a Vps13-dependent process required for complete degradation of bulky remnants of dying cells.

Drosophila rhino Encodes a Female-Specific Chromo-domain Protein That Affects Chromosome Structure and Egg Polarity

Genetics ◽  
2001 ◽  
Vol 159 (3) ◽  
pp. 1117-1134 ◽  
Author(s):  
Alison M Volpe ◽  
Heidi Horowitz ◽  
Constance M Grafer ◽  
Stephen M Jackson ◽  
Celeste A Berg
Keyword(s):  
Nurse Cell ◽  
Chromosome Structure ◽  
Nurse Cells ◽  
Embryonic Patterning ◽  
Loss Of Function ◽  
Cell Nuclei ◽  
Heterochromatin Protein 1 ◽  
Chromo Domain ◽  
Egg Chambers ◽  
Female Specific

Abstract Here we describe our analyses of Rhino, a novel member of the Heterochromatin Protein 1(HP1) subfamily of chromo box proteins. rhino (rhi) is expressed only in females and chiefly in the germline, thus providing a new tool to dissect the role of chromo-domain proteins in development. Mutations in rhi disrupt eggshell and embryonic patterning and arrest nurse cell nuclei during a stage-specific reorganization of their polyploid chromosomes, a mitotic-like state called the “five-blob” stage. These visible alterations in chromosome structure do not affect polarity by altering transcription of key patterning genes. Expression levels of gurken (grk), oskar (osk), bicoid (bcd), and decapentaplegic (dpp) transcripts are normal, with a slight delay in the appearance of bcd and dpp mRNAs. Mislocalization of grk and osk transcripts, however, suggests a defect in the microtubule reorganization that occurs during the middle stages of oogenesis and determines axial polarity. This defect likely results from aberrant Grk/Egfr signaling at earlier stages, since rhi mutations delay synthesis of Grk protein in germaria and early egg chambers. In addition, Grk protein accumulates in large, actin-caged vesicles near the endoplasmic reticulum of stages 6–10 egg chambers. We propose two hypotheses to explain these results. First, Rhi may play dual roles in oogenesis, independently regulating chromosome compaction in nurse cells at the end of the unique endoreplication cycle 5 and repressing transcription of genes that inhibit Grk synthesis. Thus, loss-of-function mutations arrest nurse cell chromosome reorganization at the five-blob stage and delay production or processing of Grk protein, leading to axial patterning defects. Second, Rhi may regulate chromosome compaction in both nurse cells and oocyte. Loss-of-function mutations block nurse cell nuclear transitions at the five-blob stage and activate checkpoint controls in the oocyte that arrest Grk synthesis and/or inhibit cytoskeletal functions. These functions may involve direct binding of Rhi to chromosomes or may involve indirect effects on pathways controlling these processes.

The role of microfilaments in cytoplasmic streaming in Drosophila follicles

1986 ◽  
Vol 80 (1) ◽  
pp. 159-169 ◽  
Author(s):  
H.O. Gutzeit
Keyword(s):  
Cell Membrane ◽  
Nuclear Membrane ◽  
Actin Filaments ◽  
Cytoplasmic Streaming ◽  
Nurse Cell ◽  
Time Lapse ◽  
Nurse Cells ◽  
Cell Nuclei ◽  
Cell Cytoplasm

During the last phase of oogenesis in Drosophila, nurse cell cytoplasm can be seen to be streaming into the growing oocyte when visualized in time-lapse films. This process can be reversibly inhibited by cytochalasins. The distribution of F-actin filaments in the nurse cells has been studied by staining with rhodamine-conjugated phalloidin. At the beginning of cytoplasmic streaming (stage 10B) increasingly thick bundles of microfilaments formed, many of which spanned the nurse cell cytoplasm from the cell membrane to the nuclear membrane. The association of F-actin with the nuclear membrane persisted when nurse cell nuclei were isolated mechanically. The experimental evidence suggests that microfilament contraction in the nurse cells leads to cytoplasmic streaming by pressure flow.

Memoirs: Certain Phenomena of Tenthredinid Oogenesis as Revealed Mainly by Feulgen's Nuclear-Reaction

1930 ◽  
Vol s2-73 (292) ◽  
pp. 617-630
Author(s):  
R.A. R. GRESSON
Keyword(s):  
Nurse Cell ◽  
Chemical Change ◽  
Follicle Cell ◽  
Nuclear Material ◽  
Methyl Blue ◽  
Follicle Cells ◽  
Nuclear Chromatin ◽  
Nurse Cells ◽  
Cell Nuclei ◽  
Nucleolar Material

1. By the use of Feulgen's ‘nuclealreaktion’ certain points of Tenthredinid oogenesis have been subjected to closer study. The chromatin of the early nurse-cells of Allantus pallipes exists in the form of granules, the majority of which occur close to the nuclear membrane. In the older cells a nuclear network appears in which is distributed granules of chromatin. In Thrinax mixta, where the ovarioles were more highly developed, the chromatin of the nurse-cells occurs as granules scattered through the nucleus; a nuclear network is not present, but certain granules appear to be connected by a thread. The granules which were shown to surround the nurse-cell nuclei (in material treated by Bensley's method and also by fixation in Bouin's picro-formol and subsequently stained in iron haematoxylin) and which were formerly regarded as chromatin emissions from the nurse-cell nuclei (9) were not revealed by Feulgen's technique. They therefore cannot be regarded as chromatin. Their precise nature and origin remains undetermined. 2. The nucleoli of the early nurse-cells of both species, as revealed by Mann's methyl-blue eosin, are faintly basophil. Later they break up into a number of basophil bodies which undergo fragmentation; formerly (technique and reference as in 1) the basophil nucleolus and the basophil bodies originating from it were termed ‘nuclear material’ undergoing fragmentation. While this basophil nucleolar material presents a fragmented appearance, it increases in amount as evidenced by the large number of basophil bodies present in the older nurse-cell nuclei. This material is utilized for the nourishment of the egg after the latter engulfs the nurse-cell nuclei. Nucleolar extrusions to the cytoplasm do not occur. 3. The behaviour of the chromatin of the follicle-cell nuclei is similar to that of the nurse-cell nuclei except that in Allantus pallipes the nuclear chromatin network as demonstrated by Feulgen's technique disappears in the older cells. 4. The nucleoli of the follicle-cells are basophil. They become broken up in the older cells, but in most cases the resulting masses remain in contact. Nucleolar extrusions to the cytoplasm do not occur. 5. The occurrence of deeply basophil material in the cytoplasm of the follicle-cells of Thrinax mixta stained with Mann's methyl-blue eosin, formerly described for Bouin fixed material stained in iron haematoxylin (9), suggests that some substance in solution may be passed into the ooplasm; extrusion of granules from the follicle-cells to the ooplasm does not take place. 6. The absence or non-visibility of chromatin (Feulgen's technique) from the oocytes of Thrinax mixta, and its disappearance from the older oocytes of Allantus pallipes , would indicate that the chromatin undergoes a chemical change during oogenesis such as suggested by Koch for Chilopods. 7. The oxyphil and basophil nucleoli of the oocytes do not react to Feulgen's technique for chromatin; this agrees with Ludford's findings for the mouse and for Limnaeastagnalis.

scholarly journals Germline Cell Death Is Inhibited byP-Element Insertions Disrupting thedcp-1/pitaNested Gene Pair in Drosophila

Genetics ◽  
2003 ◽  
Vol 165 (4) ◽  
pp. 1881-1888 ◽  
Author(s):  
Bonni Laundrie ◽  
Jeanne S Peterson ◽  
Jason S Baum ◽  
Jeffrey C Chang ◽  
Dana Fileppo ◽  
...  
Keyword(s):  
Cell Death ◽  
Nurse Cell ◽  
Zinc Finger Protein ◽  
P Element ◽  
Germline Cell ◽  
Developmentally Regulated ◽  
Developmental Abnormalities ◽  
Egg Chambers ◽  
Caspase Gene ◽  
Active Caspase

AbstractGermline cell death in Drosophila oogenesis is controlled by distinct signals. The death of nurse cells in late oogenesis is developmentally regulated, whereas the death of egg chambers during mid-oogenesis is induced by environmental stress or developmental abnormalities. P-element insertions in the caspase gene dcp-1 disrupt both dcp-1 and the outlying gene, pita, leading to lethality and defective nurse cell death in late oogenesis. By isolating single mutations in the two genes, we have found that the loss of both genes contributes to this ovary phenotype. Mutants of pita, which encodes a C2H2 zinc-finger protein, are homozygous lethal and show dumpless egg chambers and premature nurse cell death in germline clones. Early nurse cell death is not observed in the dcp-1/pita double mutants, suggesting that dcp-1+ activity is required for the mid-oogenesis cell death seen in pita mutants. dcp-1 mutants are viable and nurse cell death in late oogenesis occurs normally. However, starvation-induced germline cell death during mid-oogenesis is blocked, leading to a reduction and inappropriate nuclear localization of the active caspase Drice. These findings suggest that the combinatorial loss of pita and dcp-1 leads to the increased survival of abnormal egg chambers in mutants bearing the P-element alleles and that dcp-1 is essential for cell death during mid-oogenesis.

scholarly journals DNase II mediates a parthanatos-like developmental cell death pathway in Drosophila primordial germ cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lama Tarayrah-Ibraheim ◽  
Elital Chass Maurice ◽  
Guy Hadary ◽  
Sharon Ben-Hur ◽  
Alina Kolpakova ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Germ Cells ◽  
Nuclear Translocation ◽  
Primordial Germ Cells ◽  
Nuclear Accumulation ◽  
Dependent Manner ◽  
Dnase Ii ◽  
Cell Death Pathway ◽  
Parp 1

AbstractDuring Drosophila embryonic development, cell death eliminates 30% of the primordial germ cells (PGCs). Inhibiting apoptosis does not prevent PGC death, suggesting a divergence from the conventional apoptotic program. Here, we demonstrate that PGCs normally activate an intrinsic alternative cell death (ACD) pathway mediated by DNase II release from lysosomes, leading to nuclear translocation and subsequent DNA double-strand breaks (DSBs). DSBs activate the DNA damage-sensing enzyme, Poly(ADP-ribose) (PAR) polymerase-1 (PARP-1) and the ATR/Chk1 branch of the DNA damage response. PARP-1 and DNase II engage in a positive feedback amplification loop mediated by the release of PAR polymers from the nucleus and the nuclear accumulation of DNase II in an AIF- and CypA-dependent manner, ultimately resulting in PGC death. Given the anatomical and molecular similarities with an ACD pathway called parthanatos, these findings reveal a parthanatos-like cell death pathway active during Drosophila development.

Expression and localization of androgen receptor-interacting protein-4 in the testis

2007 ◽  
Vol 292 (2) ◽  
pp. E513-E522 ◽  
Author(s):  
Andrii Domanskyi ◽  
Fu-Ping Zhang ◽  
Mirja Nurmio ◽  
Jorma J. Palvimo ◽  
Jorma Toppari ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor ◽  
Dependent Manner ◽  
Cell Nuclei ◽  
Interacting Protein ◽  
Independent Functions

Androgen receptor-interacting protein 4 (ARIP4) belongs to the SNF2 family of proteins involved in chromatin remodeling, DNA excision repair, and homologous recombination. It is a DNA-dependent ATPase, binds to DNA and mononucleosomes, and interacts with androgen receptor (AR) and modulates AR-dependent transactivation. We have examined in this study the expression and cellular localization of ARIP4 during postnatal development of mouse testis. ARIP4 was detected by immunohistochemistry in Sertoli cell nuclei at all ages studied, starting on day 5, and exhibited the highest expression level in adult mice. At the onset of spermatogenesis, ARIP4 expression became evident in spermatogonia, pachytene, and diplotene spermatocytes. Immunoreactive ARIP4 antigen was present in Leydig cell nuclei. In Sertoli cells ARIP4 was expressed in a stage-dependent manner, with high expression levels at stages II–VI and VII–VIII. ARIP4 expression patterns did not differ significantly in testes of wild-type, follicle-stimulating hormone receptor knockout, and luteinizing hormone receptor knockout mice. In testes of hypogonadal mice, ARIP4 was found mainly in interstitial cells and exhibited lower expression in Sertoli and germ cells. In vitro stimulation of rat seminiferous tubule segments with testosterone, FSH, or forskolin did not significantly change stage-specific levels of ARIP4 mRNA. Heterozygous ARIP4+/− mice were haploinsufficient and had reduced levels of Sertoli-cell specific androgen-regulated Rhox5 (also called Pem) mRNA. Collectively, ARIP4 is an AR coregulator in Sertoli cells in vivo, but the expression in the germ cells implies that it has also AR-independent functions in spermatogenesis.

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