Faculty Opinions recommendation of ELT-5 and ELT-6 are required continuously to regulate epidermal seam cell differentiation and cell fusion in C. elegans.

2001 ◽  
Author(s):  
Bruce Bowerman
Keyword(s):  
Cell Differentiation ◽  
Cell Fusion ◽  
C Elegans ◽  
Seam Cell

ELT-5 and ELT-6 are required continuously to regulate epidermal seam cell differentiation and cell fusion inC. elegans

Development ◽  
2001 ◽  
Vol 128 (15) ◽  
pp. 2867-2880 ◽  
Author(s):  
Kyunghee Koh ◽  
Joel H. Rothman
Keyword(s):  
Cell Differentiation ◽  
Cell Fusion ◽  
Cell Types ◽  
Regulatory Elements ◽  
Epidermal Cells ◽  
Gata Factor ◽  
C Elegans ◽  
Seam Cell ◽  
Specific Regulation ◽  
The Individual

The C. elegans epidermis is a simple epithelium comprised of three major cell types, the seam, syncytial and P cells. While specification of all major epidermal cells is known to require the ELT-1 GATA transcription factor, little is known about how the individual epidermal cell types are specified. We report that elt-5 and -6, adjacent genes encoding GATA factors, are essential for the development of the lateral epidermal cells, the seam cells. Inhibition of elt-5 and -6 function by RNA-mediated interference results in penetrant late embryonic and early larval lethality. Seam cells in affected animals do not differentiate properly: the alae, seam-specific cuticular structures, are generally absent and expression of several seam-specific markers is blocked. In addition, elt-3, which encodes another GATA factor normally expressed in non-seam epidermis, is often ectopically expressed in the seam cells of affected animals, demonstrating that ELT-5 and -6 repress elt-3 expression in wild-type seam cells. Seam cells in affected animals often undergo inappropriate fusion with the epidermal syncytia. Interference of elt-5 and -6 function during larval development can cause fusion of all seam cells with the surrounding syncytia and pronounced defects in molting. elt-5 and -6 are both expressed in seam cells and many other cells, and are apparently functionally interchangeable. Their expression is controlled by separable tissue-specific regulatory elements and the apportionment of monocistronic versus dicistronic transcription of both genes appears to be subject to cell-type-specific regulation. Collectively, these findings indicate that elt-5 and -6 function continuously throughout C. elegans development to regulate seam cell differentiation and cell fusion.

scholarly journals Barrier to autointegration factor blocks premature cell fusion and maintains adult muscle integrity in C. elegans

2007 ◽  
Vol 178 (4) ◽  
pp. 661-673 ◽  
Author(s):  
Ayelet Margalit ◽  
Esther Neufeld ◽  
Naomi Feinstein ◽  
Katherine L. Wilson ◽  
Benjamin Podbilewicz ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Body Wall ◽  
Homozygous Deletion ◽  
C Elegans ◽  
Larval Stages ◽  
Double Stranded Dna ◽  
Seam Cell ◽  
Independent Mechanism ◽  
Transcription Regulators ◽  
Body Wall Muscles

Barrier to autointegration factor (BAF) binds double-stranded DNA, selected histones, transcription regulators, lamins, and LAP2–emerin–MAN1 (LEM) domain proteins. During early Caenorhabditis elegans embryogenesis, BAF-1 is required to organize chromatin, capture segregated chromosomes within the nascent nuclear envelope, and assemble lamin and LEM domain proteins in reforming nuclei. In this study, we used C. elegans with a homozygous deletion of the baf-1 gene, which survives embryogenesis and larval stages, to report that BAF-1 regulates maturation and survival of the germline, cell migration, vulva formation, and the timing of seam cell fusion. In the seam cells, BAF-1 represses the expression of the EFF-1 fusogen protein, but fusion still occurs in C. elegans lacking both baf-1 and eff-1. This suggests the existence of an eff-1–independent mechanism for cell fusion. BAF-1 is also required to maintain the integrity of specific body wall muscles in adult animals, directly implicating BAF in the mechanism of human muscular dystrophies (laminopathies) caused by mutations in the BAF-binding proteins emerin and lamin A.

A Deficiency Screen for Zygotic Loci Required for Establishment and Patterning of the Epidermis in Caenorhabditis elegans

Genetics ◽  
1997 ◽  
Vol 146 (1) ◽  
pp. 185-206 ◽  
Author(s):  
Rebecca M Terns ◽  
Peggy Kroll-Conner ◽  
Jiangwen Zhu ◽  
Sooyoun Chung ◽  
Joel H Rothman
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Types ◽  
Epidermal Cells ◽  
Epidermal Differentiation ◽  
Apparent Effect ◽  
Internal Organs ◽  
C Elegans ◽  
Seam Cell ◽  
Genomic Regions ◽  
Caenorhabditis Elegans Genome

To identify genomic regions required for establishment and patterning of the epidermis, we screened 58 deficiencies that collectively delete at least ∼67% of the Caenorhabditis elegans genome. The epidermal pattern of deficiency homozygous embryos was analyzed by examining expression of a marker specific for one of the three major epidermal cell types, the seam cells. The organization of the epidermis and internal organs was also analyzed using a monoclonal antibody specific for epithelial adherens junctions. While seven deficiencies had no apparent effect on seam cell production, 21 were found to result in subnormal, and five in excess numbers of these cells. An additional 23 deficiencies blocked expression of the seam cell marker, in some cases without preventing cell proliferation. Two deficiencies result in multinucleate seam cells. Deficiencies were also identified that result in subnormal numbers of epidermal cells, hyperfusion of epidermal cells into a large syncytium, or aberrant epidermal differentiation. Finally, analysis of internal epithelia revealed deficiencies that cause defects in formation of internal organs, including circularization of the intestine and bifurcation of the pharynx lumen. This study reveals that many regions of the C. elegans genome are required zygotically for patterning of the epidermis and other epithelia.

scholarly journals Microfluidic-based imaging of complete C. elegans larval development

2021 ◽  
Author(s):  
Simon Berger ◽  
Silvan Spiri ◽  
Andrew deMello ◽  
Alex Hajnal
Keyword(s):  
Imaging Method ◽  
Cover Glass ◽  
Vulval Development ◽  
C Elegans ◽  
Larval Stages ◽  
Seam Cell ◽  
Time Observation ◽  
On Chip ◽  
First Time

Several microfluidic-based methods for long-term C. elegans imaging have been introduced in recent years, allowing real-time observation of previously inaccessible processes. The ex-isting methods either permit imaging across multiple larval stages without maintaining a stable worm orientation, or allow for very good immobilization but are only suitable for shorter experiments. Here, we present a novel microfluidic imaging method, which allows parallel live-imaging across multiple larval stages, while delivering excellent immobilization and maintaining worm orientation and identity over time. This is achieved by employing an array of microfluidic trap channels carefully tuned to maintain worms in a stable orienta-tion, while allowing growth and molting to occur. Immobilization is supported by an active hydraulic valve, which presses worms onto the cover glass during image acquisition, with the animals remaining free for most of an experiment. Excellent quality images can be ac-quired of multiple worms in parallel, with little impact of the imaging method on worm via-bility or developmental timing. The capabilities of this methodology are demonstrated by observing the hypodermal seam cell divisions and, for the first time, the entire process of vulval development from induction to the end of morphogenesis. Moreover, we demonstrate RNAi on-chip, which allows for perturbation of dynamic developmental processes, such as basement membrane breaching during anchor cell invasion.

scholarly journals Genetic Control of Fusion Pore Expansion in the Epidermis ofCaenorhabditis elegans

2007 ◽  
Vol 18 (4) ◽  
pp. 1153-1166 ◽  
Author(s):  
Tamar Gattegno ◽  
Aditya Mittal ◽  
Clari Valansi ◽  
Ken C.Q. Nguyen ◽  
David H. Hall ◽  
...  
Keyword(s):  
Membrane Fusion ◽  
Cell Fusion ◽  
Fusion Pore ◽  
Membrane Domains ◽  
Cell Pair ◽  
C Elegans ◽  
Ultrastructural Studies ◽  
Different Temperatures ◽  
Multiple Cell ◽  
Extensive Information

Developmental cell fusion is found in germlines, muscles, bones, placentae, and stem cells. In Caenorhabditis elegans 300 somatic cells fuse during development. Although there is extensive information on the early intermediates of viral-induced and intracellular membrane fusion, little is known about late stages in membrane fusion. To dissect the pathway of cell fusion in C. elegans embryos, we use genetic and kinetic analyses using live-confocal and electron microscopy. We simultaneously monitor the rates of multiple cell fusions in developing embryos and find kinetically distinct stages of initiation and completion of membrane fusion in the epidermis. The stages of cell fusion are differentially blocked or retarded in eff-1 and idf-1 mutants. We generate kinetic cell fusion maps for embryos grown at different temperatures. Different sides of the same cell differ in their fusogenicity: the left and right membrane domains are fusion-incompetent, whereas the anterior and posterior membrane domains fuse with autonomous kinetics in embryos. All but one cell pair can initiate the formation of the largest syncytium. The first cell fusion does not trigger a wave of orderly fusions in either direction. Ultrastructural studies show that epidermal syncytiogenesis require eff-1 activities to initiate and expand membrane merger.

scholarly journals The nuclear receptor NHR-25 cooperates with the Wnt/ -catenin asymmetry pathway to control differentiation of the T seam cell in C. elegans

2009 ◽  
Vol 122 (17) ◽  
pp. 3051-3060 ◽  
Author(s):  
M. Hajduskova ◽  
M. Jindra ◽  
M. A. Herman ◽  
M. Asahina
Keyword(s):  
Nuclear Receptor ◽  
C Elegans ◽  
Seam Cell

Zygote giant cell differentiation in Dictyostelium discoideum: biochemical markers of specific stages of sexual development

1992 ◽  
Vol 70 (10-11) ◽  
pp. 1200-1208 ◽  
Author(s):  
Darren D. Browning ◽  
Keith E. Lewis ◽  
Danton H. O'Day
Keyword(s):  
Alkaline Phosphatase ◽  
Cell Differentiation ◽  
Giant Cell ◽  
Dictyostelium Discoideum ◽  
Cell Fusion ◽  
Sexual Development ◽  
Giant Cells ◽  
Second Phase ◽  
Developmental Phase ◽  
Calcium Dependent

Sexual development in Dictyostelium discoideum has many unique features making it an attractive eukaryotic model system for the study of biomembrane fusion and intercellular communication. The work presented here provides primary biochemical evidence for two distinct phases during early sexual development that appear to be defined by calcium-dependent gamete cell fusion. In addition, we introduce a novel procedure for the enrichment of zygote giant cells and use this method to define certain wheat-germ agglutinin binding glycoproteins which are specifically located in zygote giant cells and others which are markers for surrounding amoebae in the second phase of development. In addition, a G protein which is present in high amounts early in development is unique to giant cells in the second phase, suggesting a role in phagocytosis. Finally, alkaline phosphatase activity was found to mark the first phase of sexual development, suggesting a role in cell fusion. This contrasts with the patterns of α-mannosidase and β-glucosidase activity that increase late in the second developmental phase, where they likely function in endocyte digestion during the cytophagic period. The developmental significance of these findings is discussed.Key words: zygote giant cell differentiation, Ca2+, glycoproteins, GTP-binding proteins, alkaline phosphatase, glycosidase, cell fusion.

scholarly journals Untwisting the Caenorhabditis elegans embryo

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Ryan Patrick Christensen ◽  
Alexandra Bokinsky ◽  
Anthony Santella ◽  
Yicong Wu ◽  
Javier Marquina-Solis ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Tracking ◽  
Positional Information ◽  
Supplementary File ◽  
Cell Nuclei ◽  
C Elegans ◽  
Seam Cell ◽  
Late Embryogenesis ◽  
Embryonic Nervous System ◽  
Supplementary Material

The nematode Caenorhabditis elegans possesses a simple embryonic nervous system with few enough neurons that the growth of each cell could be followed to provide a systems-level view of development. However, studies of single cell development have largely been conducted in fixed or pre-twitching live embryos, because of technical difficulties associated with embryo movement in late embryogenesis. We present open-source untwisting and annotation software (http://mipav.cit.nih.gov/plugin_jws/mipav_worm_plugin.php) that allows the investigation of neurodevelopmental events in late embryogenesis and apply it to track the 3D positions of seam cell nuclei, neurons, and neurites in multiple elongating embryos. We also provide a tutorial describing how to use the software (<xref ref-type="supplementary-material" rid="SD1-data">Supplementary file 1</xref>) and a detailed description of the untwisting algorithm (Appendix). The detailed positional information we obtained enabled us to develop a composite model showing movement of these cells and neurites in an 'average' worm embryo. The untwisting and cell tracking capabilities of our method provide a foundation on which to catalog C. elegans neurodevelopment, allowing interrogation of developmental events in previously inaccessible periods of embryogenesis.

scholarly journals unc-37/Groucho and lsy-22/AES repress Wnt target genes in C. elegans asymmetric cell divisions

2022 ◽  
Author(s):  
Kimberly N. Bekas ◽  
Bryan T. Phillips
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Target Gene ◽  
Target Genes ◽  
Intermediate Cell ◽  
Beta Catenin ◽  
Cell Fate Decisions ◽  
C Elegans ◽  
Somatic Gonad ◽  
Seam Cell

Asymmetric cell division (ACD) is a fundamental mechanism of developmental cell fate specification and adult tissue homeostasis. In C. elegans, the Wnt/beta-catenin asymmetry (WβA) pathway regulates ACDs throughout embryonic and larval development. Under control of Wnt ligand-induced polarity, the transcription factor TCF/POP-1 functions with the coactivator beta-catenin/SYS-1 to activate gene expression in the signaled cell or, in absence of the coactivator, to repress Wnt target genes in the nascent unsignaled daughter cell. To date, a broad investigation of Groucho function in WβA is lacking and the function of the short Groucho AES homolog, lsy-22 has only been evaluated in C. elegans neuronal cell fate decisions. Further, there is conflicting evidence showing TCF utilizing Groucho-mediated repression may be either aided or repressed by addition of AES subfamily of Groucho proteins. Here we demonstrate a genetic interaction between Groucho repressors and TCF/POP-1 in ACDs in the somatic gonad, the seam hypodermal stem cell lineage and the early embryo. Specifically, in the somatic gonad lineage, the signaled cell fate increases after individual and double Groucho loss of function, representing the first demonstration of Groucho function in wild-type WβA ACD. Further, WβA target gene misexpression occurs at a higher rate than DTC fate changes, suggesting derepression generates an intermediate cell fate. In seam cell ACD, loss of Groucho unc-37 or Groucho-like lsy-22 in a pop-1(RNAi) hypomorphic background enhances a pop-1 seam cell expansion and target gene misregulation. Moreover, while POP-1 depletion in lsy-22 null mutants yielded an expected increase in seam cells we observed a surprising seam cell decrease in the unc-37 null subjected to POP-1 depletion. This phenotype may be due to UNC-37 regulation of pop-1 expression in this tissue since we find misregulation of POP-1 in unc-37 mutants. Lastly, Groucho functions in embryonic endoderm development since we observe ectopic endoderm target gene expression in lsy-22(ot244) heterozygotes and unc-37(tm4649) heterozygotes subjected to intermediate levels of hda-1(RNAi). Together, these data indicate Groucho repressor modulation of cell fate via regulation of POP-1/TCF repression is widespread in asymmetric cell fate decisions and suggests a novel role of LSY-22 as a bona fide TCF repressor. As AES Grouchos are well-conserved, our model of combinatorial TCF repression by both Gro/TLE and AES warrants further investigation. 

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