scholarly journals Nuclear positioning in the gonadal distal tip cells of C. elegans

Worm ◽  
2012 ◽  
Vol 1 (2) ◽  
pp. 112-115 ◽  
Author(s):  
Hon-Song Kim ◽  
Kiyoji Nishiwaki
Keyword(s):  
Nuclear Positioning ◽  
C Elegans ◽  
Distal Tip Cells ◽  
Tip Cells

scholarly journals Chondroitin acts in the guidance of gonadal distal tip cells in C. elegans

2006 ◽  
Vol 300 (2) ◽  
pp. 635-646 ◽  
Author(s):  
Norio Suzuki ◽  
Hidenao Toyoda ◽  
Mitsue Sano ◽  
Kiyoji Nishiwaki
Keyword(s):  
C Elegans ◽  
Distal Tip Cells ◽  
Tip Cells

C. elegans as a model system to study the function of the COG complex in animal development

2006 ◽  
Vol 387 (8) ◽  
pp. 1031-1035 ◽  
Author(s):  
Yukihiko Kubota ◽  
Kiyoji Nishiwaki
Keyword(s):  
Golgi Apparatus ◽  
Complex Function ◽  
Model System ◽  
Secreted Proteins ◽  
Animal Development ◽  
C Elegans ◽  
Cog Complex ◽  
Family Protein ◽  
Distal Tip Cells ◽  
Tip Cells

AbstractThe conserved oligomeric Golgi (COG) complex is an octameric protein complex associated with the Golgi apparatus and is required for proper sorting and glycosylation of Golgi resident enzymes and secreted proteins. Although COG complex function has been extensively studied at the cellular and subcellular levels, its role in animal development mostly remains unknown. Recently, mutations in the components of the COG complex were found to cause abnormal gonad morphogenesis inCaenorhabditis elegans. InC. elegans, the COG complex acts in the glycosylation of an ADAM (a disintegrin and metalloprotease) family protein, MIG-17, which directs migration of gonadal distal tip cells to lead gonad morphogenesis. This is the first link between the COG complex and the function of an ADAM protease that is directly involved in organ morphogenesis, demonstrating the potential ofC. elegansas a model system to study COG function in animal development.

Regulation of the UNC-5 netrin receptor initiates the first reorientation of migrating distal tip cells in Caenorhabditis elegans

Development ◽  
2000 ◽  
Vol 127 (3) ◽  
pp. 585-594 ◽  
Author(s):  
M. Su ◽  
D.C. Merz ◽  
M.T. Killeen ◽  
Y. Zhou ◽  
H. Zheng ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Developmental Stage ◽  
Phase 1 ◽  
Critical Role ◽  
The Body ◽  
Dependent Manner ◽  
C Elegans ◽  
Guidance Cue ◽  
Distal Tip Cells ◽  
Tip Cells

Cell migrations play a critical role in animal development and organogenesis. Here, we describe a mechanism by which the migration behaviour of a particular cell type is regulated temporally and coordinated with over-all development of the organism. The hermaphrodite distal tip cells (DTCs) of Caenorhabditis elegans migrate along the body wall in three sequential phases distinguished by the orientation of their movements, which alternate between the anteroposterior and dorsoventral axes. The ventral-to-dorsal second migration phase requires the UNC-6 netrin guidance cue and its receptors UNC-5 and UNC-40, as well as additional, UNC-6-independent guidance systems. We provide evidence that the transcriptional upregulation of unc-5 in the DTCs is coincident with the initiation of the second migration phase, and that premature UNC-5 expression in these cells induces precocious turning in an UNC-6-dependent manner. The DAF-12 steroid hormone receptor, which regulates developmental stage transitions in C. elegans, is required for initiating the first DTC turn and for coincident unc-5 upregulation. We also present evidence for the existence of a mechanism that opposes or inhibits UNC-5 function during the longitudinal first migration phase and for a mechanism that facilitates UNC-5 function during turning. The facilitating mechanism presumably does not involve transcriptional regulation of unc-5 but may represent an inhibition of the phase 1 mechanism that opposes or inhibits UNC-5. These results, therefore, reveal the existence of two mechanisms that regulate the UNC-5 receptor that are critical for responsiveness to the UNC-6 netrin guidance cue and for linking the directional guidance of migrating distal tip cells to developmental stage advancements.

scholarly journals C. elegans Agrin Is Expressed in Pharynx, IL1 Neurons and Distal Tip Cells and Does Not Genetically Interact with Genes Involved in Synaptogenesis or Muscle Function

PLoS ONE ◽  
2007 ◽  
Vol 2 (8) ◽  
pp. e731 ◽  
Author(s):  
Ana Hrus ◽  
Gordon Lau ◽  
Harald Hutter ◽  
Susanne Schenk ◽  
Jacqueline Ferralli ◽  
...  
Keyword(s):  
Muscle Function ◽  
C Elegans ◽  
Distal Tip Cells ◽  
Tip Cells

scholarly journals Genetic interactions among ADAMTS metalloproteases and basement membrane molecules in cell migration in Caenorhabditis elegans

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0240571
Author(s):  
Ayaka Imanishi ◽  
Yuma Aoki ◽  
Masaki Kakehi ◽  
Shunsuke Mori ◽  
Tomomi Takano ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Basement Membrane ◽  
Collagen Iv ◽  
Wild Type ◽  
Suppressor Mutations ◽  
Genetic Suppressors ◽  
Basement Membrane Protein ◽  
Distal Tip Cells ◽  
Tip Cells ◽  
Shaped Pattern

During development of the Caenorhabditis elegans gonad, the gonadal leader cells, called distal tip cells (DTCs), migrate in a U-shaped pattern to form the U-shaped gonad arms. The ADAMTS (a disintegrin and metalloprotease with thrombospondin motifs) family metalloproteases MIG-17 and GON-1 are required for correct DTC migration. Mutations in mig-17 result in misshapen gonads due to the misdirected DTC migration, and mutations in gon-1 result in shortened and swollen gonads due to the premature termination of DTC migration. Although the phenotypes shown by mig-17 and gon-1 mutants are very different from one another, mutations that result in amino acid substitutions in the same basement membrane protein genes, emb-9/collagen IV a1, let-2/collagen IV a2 and fbl-1/fibulin-1, were identified as genetic suppressors of mig-17 and gon-1 mutants. To understand the roles shared by these two proteases, we examined the effects of the mig-17 suppressors on gon-1 and the effects of the gon-1 suppressors and enhancers on mig-17 gonadal defects. Some of the emb-9, let-2 and fbl-1 mutations suppressed both mig-17 and gon-1, whereas others acted only on mig-17 or gon-1. These results suggest that mig-17 and gon-1 have their specific functions as well as functions commonly shared between them for gonad formation. The levels of collagen IV accumulation in the DTC basement membrane were significantly higher in the gon-1 mutants as compared with wild type and were reduced to the wild-type levels when combined with suppressor mutations, but not with enhancer mutations, suggesting that the ability to reduce collagen IV levels is important for gon-1 suppression.

scholarly journals A network of nuclear envelope proteins and cytoskeletal force generators mediates movements of and within nuclei throughout Caenorhabditis elegans development

2019 ◽  
Vol 244 (15) ◽  
pp. 1323-1332 ◽  
Author(s):  
Daniel A Starr
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Nuclear Envelope ◽  
Nuclear Membrane ◽  
Dna Damage Repair ◽  
Nuclear Migration ◽  
Envelope Proteins ◽  
Nuclear Positioning ◽  
C Elegans ◽  
Damage Repair

Nuclear migration and anchorage, together referred to as nuclear positioning, are central to many cellular and developmental events. Nuclear positioning is mediated by a conserved network of nuclear envelope proteins that interacts with force generators in the cytoskeleton. At the heart of this network are linker of nucleoskeleton and cytoskeleton (LINC) complexes made of Sad1 and UNC-84 (SUN) proteins at the inner nuclear membrane and Klarsicht, ANC-1, and Syne homology (KASH) proteins in the outer nuclear membrane. LINC complexes span the nuclear envelope, maintain nuclear envelope architecture, designate the surface of nuclei distinctly from the contiguous endoplasmic reticulum, and were instrumental in the early evolution of eukaryotes. LINC complexes interact with lamins in the nucleus and with various cytoplasmic KASH effectors from the surface of nuclei. These effectors regulate the cytoskeleton, leading to a variety of cellular outputs including pronuclear migration, nuclear migration through constricted spaces, nuclear anchorage, centrosome attachment to nuclei, meiotic chromosome movements, and DNA damage repair. How LINC complexes are regulated and how they function are reviewed here. The focus is on recent studies elucidating the best-understood network of LINC complexes, those used throughout Caenorhabditis elegans development. Impact statement Defects in nuclear positioning disrupt development in many mammalian tissues. In human development, LINC complexes play important cellular functions including nuclear positioning, homolog pairing in meiosis, DNA damage repair, wound healing, and gonadogenesis. The topics reviewed here are relevant to public health because defects in nuclear positioning and mutations in LINC components are associated with a wide variety of human diseases including muscular dystrophies, neurological disorders, progeria, aneurysms, hearing loss, blindness, sterility, and multiple cancers. Although this review focuses on findings in the model nematode Caenorhabditis elegans, the studies are relevant because almost all the findings originally made in C. elegans are conserved to humans. Furthermore, C. elegans remains the best described network for how LINC complexes are regulated and function.

Mutations Affecting Symmetrical Migration of Distal Tip Cells in Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (3) ◽  
pp. 985-997 ◽  
Author(s):  
Kiyoji Nishiwaki
Keyword(s):  
Caenorhabditis Elegans ◽  
Rotational Symmetry ◽  
The Other ◽  
Body Region ◽  
Distal Tip Cells ◽  
Complementation Groups ◽  
Mutant Phenotypes ◽  
Tip Cells ◽  
Posterior Body Region ◽  
Null Mutants

Abstract The rotational symmetry of the Caenorhabditis elegans gonad arms is generated by the symmetrical migration of two distal tip cells (DTCs), located on the anterior and posterior ends of the gonad primordium. Mutations that cause asymmetrical migration of the two DTCs were isolated. All seven mutations were recessive and assigned to six different complementation groups. vab-3(k121) and vab-3(k143) affected anterior DTC migration more frequently than posterior, although null mutants showed no bias. The other five mutations, mig-14(k124), mig-17(k113), mig-18(k140), mig-19(k142), and mig-20(k148), affected posterior DTC migration more frequently than anterior. These observations imply that the migration of each DTC is regulated differently. mig-14 and mig-19 also affected the migration of other cells in the posterior body region. Four distinct types of DTC migration abnormalities were defined on the basis of the mutant phenotypes. vab-3; mig-14 double mutants exhibited the types of DTC migration defects seen for vab-3 single mutants. Combination of mig-17 and mig-18 or mig-19, which are characterized by the same types of posterior DTC migration defects, exhibited strong enhancement of anterior DTC migration defects, suggesting that they affect the same or parallel pathways regulating anterior DTC migration.

scholarly journals The Nesprin-1/-2 ortholog ANC-1 regulates organelle positioning in C. elegans without its KASH or actin-binding domains

2020 ◽  
Author(s):  
Hongyan Hao ◽  
Shilpi Kalra ◽  
Laura E. Jameson ◽  
Leslie A. Guerrero ◽  
Natalie E. Cain ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Nuclear Membrane ◽  
Actin Binding ◽  
Nuclear Positioning ◽  
Outer Nuclear Membrane ◽  
Calponin Homology ◽  
C Elegans ◽  
Binding Domains ◽  
Null Phenotype ◽  
Er Membrane

AbstractKASH proteins in the outer nuclear membrane comprise the cytoplasmic half of LINC complexes that connect nuclei to the cytoskeleton. Caenorhabditis elegans ANC-1, an ortholog of Nesprin-1/2, contains actin-binding and KASH domains at opposite ends of a long spectrin-like region. Deletion of either the KASH or calponin homology (CH) domains does not completely disrupt nuclear positioning, suggesting neither KASH nor CH domains are essential. Deletions in the spectrin-like region of ANC-1 led to significant defects, but only recapitulated the null phenotype in combination with mutations in the trans-membrane span. In anc-1 mutants, the ER was unanchored, moving throughout the cytoplasm, and often fragmented. The data presented here support a cytoplasmic integrity model where ANC-1 localizes to the ER membrane and extends into the cytoplasm to position nuclei, ER, mitochondria, and likely other organelles in place.

A tissue-specific knock-out strategy reveals that lin-26 is required for the formation of the somatic gonad epithelium in Caenorhabditis elegans

Development ◽  
1998 ◽  
Vol 125 (16) ◽  
pp. 3213-3224 ◽  
Author(s):  
B.G. den Boer ◽  
S. Sookhareea ◽  
P. Dufourcq ◽  
M. Labouesse
Keyword(s):  
Caenorhabditis Elegans ◽  
Null Mutant ◽  
Similar Function ◽  
Knock Out ◽  
Somatic Gonad ◽  
Distal Tip Cells ◽  
Germline Proliferation ◽  
Tip Cells ◽  
New Alleles ◽  
Lineage Analysis

The Caenorhabditis elegans LIN-26 protein is required to specify and/or maintain the fates of all non-neuronal ectodermal cells. Here we show that lin-26 is expressed until the somatic gonad primordium stage in all cells of the somatic gonad, except in distal tip cells, and later in all uterine cells. To determine if lin-26 functions in the somatic gonad, we have generated gonad-specific lin-26 alleles obtained by integration of lin-26 promoter deletion derivatives into a lin-26 null mutant background. In this way, we rescued the lethal phenotype imparted by lin-26 null mutations and uncovered a highly penetrant sterile phenotype. Specifically, the strongest of these new alleles was characterized by the absence of lin-26 expression in the somatic gonad, the presence of endomitotic oocytes, decreased germline proliferation, a protruding vulva and a less penetrant absence of gonad arms. Lineage analysis of mutant somatic gonads and examination of several markers expressed in the spermatheca, sheath cells, distal tip cells and the uterus, suggest that LIN-26 is required in sheath, spermatheca and uterine precursors, and in uterine cells. We conclude that lin-26 performs a similar function in the non-neuronal ectoderm and the somatic gonad, a mesoderm derivative, and we speculate that lin-26 is required to express epithelial characteristics.

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