scholarly journals Up-regulation of the Ku heterodimer inDrosophilatesticular cyst cells

FEBS Letters ◽  
2007 ◽  
Vol 581 (9) ◽  
pp. 1707-1715 ◽  
Author(s):  
Alexander M. Boutanaev ◽  
Lyudmila M. Mikhaylova ◽  
Dmitry I. Nurminsky
Keyword(s):  
Cyst Cells

scholarly journals The actin-binding protein profilin is required for germline stem cell maintenance and germ cell enclosure by somatic cyst cells

Development ◽  
2013 ◽  
Vol 141 (1) ◽  
pp. 73-82 ◽  
Author(s):  
A. R. Shields ◽  
A. C. Spence ◽  
Y. M. Yamashita ◽  
E. L. Davies ◽  
M. T. Fuller
Keyword(s):  
Stem Cell ◽  
Germ Cell ◽  
Binding Protein ◽  
Actin Binding ◽  
Germline Stem Cell ◽  
Actin Binding Protein ◽  
Stem Cell Maintenance ◽  
Cyst Cells ◽  
Cell Maintenance

scholarly journals Probing spermatogenesis in Drosophila with P-element enhancer detectors

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 89-98 ◽  
Author(s):  
P. Gonczy ◽  
S. Viswanathan ◽  
S. DiNardo
Keyword(s):  
Germ Line ◽  
Expression Patterns ◽  
Cell Types ◽  
P Element ◽  
Structural Reorganization ◽  
Germ Cell Differentiation ◽  
Distinct Cell ◽  
Morphological Criteria ◽  
Cyst Cells ◽  
A Cell

Formation of motile sperm in Drosophila melanogaster requires the coordination of processes such as stem cell division, mitotic and meiotic control and structural reorganization of a cell. Proper execution of spermatogenesis entails the differentiation of cells derived from two distinct embryonic lineages, the germ line and the somatic mesoderm. Through an analysis of homozygous viable and fertile enhancer detector lines, we have identified molecular markers for the different cell types present in testes. Some lines label germ cells or somatic cyst cells in a stage-specific manner during their differentiation program. These expression patterns reveal transient identities for the cyst cells that had not been previously recognized by morphological criteria. A marker line labels early stages of male but not female germ cell differentiation and proves useful in the analysis of germ line sex-determination. Other lines label the hub of somatic cells around which germ line stem cells are anchored. By analyzing the fate of the somatic hub in an agametic background, we show that the germ line plays some role in directing its size and its position in the testis. We also describe how marker lines enable us to identify presumptive cells in the embryonic gonadal mesoderm before they give rise to morphologically distinct cell types. Finally, this collection of marker lines will allow the characterization of genes expressed either in the germ line or in the soma during spermatogenesis.

scholarly journals Human ADPKD primary cyst epithelial cells with a novel, single codon deletion in the PKD1 gene exhibit defective ciliary polycystin localization and loss of flow-induced Ca2+ signaling

2007 ◽  
Vol 292 (3) ◽  
pp. F930-F945 ◽  
Author(s):  
Chang Xu ◽  
Sandro Rossetti ◽  
Lianwei Jiang ◽  
Peter C. Harris ◽  
Ursa Brown-Glaberman ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nk Cells ◽  
Coiled Coil ◽  
Human Kidney ◽  
Coiled Coil Domain ◽  
Normal Human Kidney ◽  
Cyst Cells ◽  
Localization Signal ◽  
Normal Human ◽  
Autosomal Dominant Polycystic Kidney

Autosomal dominant polycystic kidney disease (ADPKD) gene products polycystin-1 (PC1) and polycystin-2 (PC2) colocalize in the apical monocilia of renal epithelial cells. Mouse and human renal cells without PC1 protein show impaired ciliary mechanosensation, and this impairment has been proposed to promote cystogenesis. However, most cyst epithelia of human ADPKD kidneys appear to express full-length PC1 and PC2 in normal or increased abundance. We show that confluent primary ADPKD cyst cells with the novel PC1 mutation ΔL2433 and with normal abundance of PC1 and PC2 polypeptides lack ciliary PC1 and often lack ciliary PC2, whereas PC1 and PC2 are both present in cilia of confluent normal human kidney (NK) epithelial cells in primary culture. Confluent NK cells respond to shear stress with transient increases in cytoplasmic Ca2+ concentration ([Ca2+]i), dependent on both extracellular Ca2+ and release from intracellular stores. In contrast, ADPKD cyst cells lack flow-sensitive [Ca2+]i signaling and exhibit reduced endoplasmic reticulum Ca2+ stores and store-depletion-operated Ca2+ entry but retain near-normal [Ca2+]i responses to ANG II and to vasopressin. Expression of wild-type and mutant CD16.7-PKD1(115–226) fusion proteins reveals within the COOH-terminal 112 amino acids of PC1 a coiled-coil domain-independent ciliary localization signal. However, the coiled-coil domain is required for CD16.7-PKD1(115–226) expression to accelerate decay of the flow-induced Ca2+ signal in NK cells. These data provide evidence for ciliary dysfunction and polycystin mislocalization in human ADPKD cells with normal levels of PC1.

scholarly journals Attenuated, flow-induced ATP release contributes to absence of flow-sensitive, purinergic Cai2+ signaling in human ADPKD cyst epithelial cells

2009 ◽  
Vol 296 (6) ◽  
pp. F1464-F1476 ◽  
Author(s):  
Chang Xu ◽  
Boris E. Shmukler ◽  
Katherine Nishimura ◽  
Elzbieta Kaczmarek ◽  
Sandro Rossetti ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Atp Hydrolysis ◽  
Atp Release ◽  
Extracellular Atp ◽  
Mrna Levels ◽  
Normal Cells ◽  
Altered Expression ◽  
Cyst Cells ◽  
Autosomal Dominant Polycystic Kidney ◽  
Renal Tubular

Flow-induced cytosolic Ca2+ Cai2+ signaling in renal tubular epithelial cells is mediated in part through P2 receptor (P2R) activation by locally released ATP. The ability of P2R to regulate salt and water reabsorption has suggested a possible contribution of ATP release and paracrine P2R activation to cystogenesis and/or enlargement in autosomal dominant polycystic kidney disease (ADPKD). We and others have demonstrated in human ADPKD cyst cells the absence of flow-induced Cai2+ signaling exhibited by normal renal epithelial cells. We now extend these findings to primary and telomerase-immortalized normal and ADPKD epithelial cells of different genotype and of both proximal and distal origins. Flow-induced elevation of Cai2+ concentration ([Ca2+]i) was absent from ADPKD cyst cells, but in normal cells was mediated by flow-sensitive ATP release and paracrine P2R activation, modulated by ecto-nucleotidase activity, and abrogated by P2R inhibition or extracellular ATP hydrolysis. In contrast to the elevated ATP release from ADPKD cells in static isotonic conditions or in hypotonic conditions, flow-induced ATP release from cyst cells was lower than from normal cells. Extracellular ATP rapidly reduced thapsigargin-elevated [Ca2+]i in both ADPKD cyst and normal cells, but cyst cells lacked the subsequent, slow, oxidized ATP-sensitive [Ca2+]i recovery present in normal cells. Telomerase-immortalized cyst cells also exhibited altered CD39 and P2X7 mRNA levels. Thus the loss of flow-induced, P2R-mediated Cai2+ signaling in human ADPKD cyst epithelial cells was accompanied by reduced flow-sensitive ATP release, altered purinergic regulation of store-operated Ca2+ entry, and altered expression of gene products controlling extracellular nucleotide signaling.

scholarly journals Drosophila melanogaster NEP2 is a new soluble member of the neprilysin family of endopeptidases with implications for reproduction and renal function

2005 ◽  
Vol 386 (2) ◽  
pp. 357-366 ◽  
Author(s):  
Josie E. THOMAS ◽  
Caroline M. RYLETT ◽  
Ahmet CARHAN ◽  
Nicholas D. BLAND ◽  
Richard J. BINGHAM ◽  
...  
Keyword(s):  
Renal Function ◽  
Drosophila Melanogaster ◽  
Renal Tubules ◽  
Large Expansion ◽  
Evolutionarily Conserved ◽  
Cyst Cells ◽  
Structural Differences ◽  
And Function ◽  
Restricted Pattern ◽  
Binding Subsites

The mammalian neprilysin (NEP) family members are typically type II membrane endopeptidases responsible for the activation/inactivation of neuropeptides and peptide hormones. Differences in substrate specificity and subcellular localization of the seven mammalian NEPs contribute to their functional diversity. The sequencing of the Drosophila melanogaster genome has revealed a large expansion of this gene family, resulting in over 20 fly NEP-like genes, suggesting even greater diversity in structure and function than seen in mammals. We now report that one of these genes (Nep2) codes for a secreted endopeptidase with a highly restricted pattern of expression. D. melanogaster NEP2 is expressed in the specialized stellate cells of the renal tubules and in the cyst cells that surround the elongating spermatid bundles in adult testis, suggesting roles for the peptidase in renal function and in spermatogenesis. D. melanogaster NEP2 was found in vesicle-like structures in the syncytial cytoplasm of the spermatid bundles, suggesting that the protein was acquired by endocytosis of protein secreted from the cyst cells. Expression of NEP2 cDNA in D. melanogaster S2 cells confirmed that the peptidase is secreted and is only weakly inhibited by thiorphan, a potent inhibitor of human NEP. D. melanogaster NEP2 also differs from human NEP in the manner in which the peptidase cleaves the tachykinin, GPSGFYGVR-amide. Molecular modelling suggests that there are important structural differences between D. melanogaster NEP2 and human NEP in the S1′ and S2′ ligand-binding subsites, which might explain the observed differences in inhibitor and substrate specificities. A soluble isoform of a mouse NEP-like peptidase is strongly expressed in spermatids, suggesting an evolutionarily conserved role for a soluble endopeptidase in spermatogenesis.

scholarly journals Stem cells commit to differentiation following multiple induction events in the Drosophila testis.

2021 ◽  
Author(s):  
Marc Amoyel ◽  
Alice C Yuen ◽  
Kenzo-Hugo Hillion
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Germ Cells ◽  
Intercellular Communication ◽  
Self Renewal ◽  
Tor Pathway ◽  
Daughter Cells ◽  
Cyst Cells ◽  
Drosophila Testis ◽  
Primed State

How and when potential becomes restricted in differentiating stem cell daughters is poorly understood. While it is thought that signals from the niche are actively required to prevent differentiation, another model proposes that stem cells can reversibly transit between multiple states, some of which are primed, but not committed, to differentiate. In the Drosophila testis, somatic cyst stem cells (CySCs) generate cyst cells, which encapsulate the germline to support its development. We find that CySCs are maintained independently of niche self-renewal signals if activity of the PI3K/Tor pathway is inhibited. Conversely, PI3K/Tor is not sufficient alone to drive differentiation, suggesting that it acts to license cells for differentiation. Indeed, we find that the germline is required for differentiation of CySCs in response to PI3K/Tor elevation, indicating that final commitment to differentiation involves several steps and intercellular communication. We propose that CySC daughter cells are plastic, that their fate depends on the availability of neighbouring germ cells, and that PI3K/Tor acts to induce a primed state for CySC daughters to enable coordinated differentiation with the germline.

scholarly journals Symmetry breaking in the female germline cyst

2021 ◽  
Author(s):  
Dmitry Nashchekin ◽  
Lara Busby ◽  
Maximilian Jacobs ◽  
Iolo Squires ◽  
Daniel St Johnston
Keyword(s):  
Symmetry Breaking ◽  
Molecular Mechanism ◽  
Microtubule Network ◽  
Cyst Cells ◽  
Germline Cyst ◽  
Dependent Transport ◽  
Branched Structure ◽  
Female Germline ◽  
Number Of Cells ◽  
Oocyte Selection

In mammals and flies, only a limited number of cells in a multicellular female germline cyst become oocytes, but how the oocyte is selected is unknown. Here we show that the microtubule minus end-stabilizing protein, Patronin/CAMSAP marks the future Drosophila oocyte and is required for oocyte specification. The spectraplakin, Shot, recruits Patronin to the fusome, a branched structure extending into all cyst cells. Patronin stabilizes more microtubules in the cell with most fusome and this weak asymmetry is amplified by Dynein-dependent transport of Patronin-stabilized microtubules. This forms a polarized microtubule network, along which Dynein transports oocyte determinants into the presumptive oocyte. Thus, Patronin amplifies a weak fusome anisotropy to break cyst symmetry. These findings reveal a molecular mechanism of oocyte selection in the germline cyst.

scholarly journals Skin Cyst: A Pathological Dead-End With a New Twist of Morphogenetic Potentials in Organoid Cultures

2021 ◽  
Vol 8 ◽  
Author(s):  
Weiming Qiu ◽  
Pei-Rong Gu ◽  
Cheng-Ming Chuong ◽  
Mingxing Lei
Keyword(s):  
Stem Cell ◽  
Transient State ◽  
Cyst Formation ◽  
Common Structure ◽  
Cellular Events ◽  
Pathological Conditions ◽  
Dead End ◽  
Cyst Cells ◽  
Organoid Cultures ◽  
Normal Architecture

A cyst is a closed sac-like structure in which cyst walls wrap certain contents typically including air, fluid, lipid, mucous, or keratin. Cyst cells can retain multipotency to regenerate complex tissue architectures, or to differentiate. Cysts can form in and outside the skin due to genetic problems, errors in embryonic development, cellular defects, chronic inflammation, infections, blockages of ducts, parasites, and injuries. Multiple types of skin cysts have been identified with different cellular origins, with a common structure including the outside cyst wall engulfs differentiated suprabasal layers and keratins. The skin cyst is usually used as a sign in pathological diagnosis. Large or surfaced skin cysts affect patients’ appearance and may cause the dysfunction or accompanying diseases of adjacent tissues. Skin cysts form as a result of the degradation of skin epithelium and appendages, retaining certain characteristics of multipotency. Surprisingly, recent organoid cultures show the formation of cyst configuration as a transient state toward more morphogenetic possibility. These results suggest, if we can learn more about the molecular circuits controlling upstream and downstream cellular events in cyst formation, we may be able to engineer stem cell cultures toward the phenotypes we wish to achieve. For pathological conditions in patients, we speculate it may also be possible to guide the cyst to differentiate or de-differentiate to generate structures more akin to normal architecture and compatible with skin homeostasis.

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