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Expr4504
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MRG-1 is highly enriched in nuclei and concentrated on chromatin. In early embryos, MRG-1 is present in the nuclei of all blastomeres. In late embryos and young larvae, MRG-1 staining is higher in the nuclei of the two primordial germ cells, Z2 and Z3, than in somatic blastomeres. In larvae and adults, MRG-1 staining is seen primarily in the nuclei of germ cells, although it is also faintly visible in the nuclei of several somatic cell types, including intestinal cells. In the adult germ line, all germ nuclei in the mitotic and meiotic regions are stained. These results demonstrate that MRG-1 is present in the germ line at all stages of development and is maternally loaded into embryos. In addition, zygotically expressed MRG-1 is produced in all cells by at least the 100-cell stage; it accumulates to higher levels in the primordial germ cells than in somatic tissues. |
Expressed in nuclei. |
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INX-3 detected during very early stages of development is likely to be maternally derived, since INX-3::GFP expressed zygotically is first detected by anti-GFP antibodies at approximately the 28-cell stage. |
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Expr2546
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At the late first larval (L1) stage, INX-3 is present transiently in some newly generated cells. The postembryonic motor neurons, descendants of the Pn.a cells, express INX-3 briefly. INX-3 is also detected briefly in cells of the first two divisions of the M blast cell, coelomocytes, and sex muscles. By the comma stage, corresponding to early embryonic morphogenesis, INX-3 is still broadly expressed, but the pattern of expression becomes more restricted as morphogenesis proceeds. Because INX-3 is localized principally in puncta at plasma membranes, it is hard to assign expression unambiguously to individual cells; however, expression in major cell types or organs is clear. Double-labeling embryos with anti-INX-3 and MH27, a mAb that binds AJM-1 in apical epithelial intercellular junctions, indicated that, at the comma stage, INX-3 is localized to the developing intestine, pharynx, and hypodermis (epidermis), at minimum. During late morphogenesis, from the 3-fold stage until hatching, INX-3 is found principally in the posterior pharynx (isthmus and terminal bulb), at the anteriormost tip of the pharynx, in the region of the posterior intestine (probably intestinal muscles or rectal cells) and in the hypodermis. Expression in these tissues continues throughout development into adulthood with the exception of the hypodermis. Hypodermal expression is strong at the time of hatching, and INX-3 is present in plaques at the intercellular boundaries between most hypodermal cells except at the ventral midline between paired P cells; however, INX-3 becomes undetectable in the hypodermis shortly after hatching. INX-3 protein is first detected at the embryonic 2-cell stage. It is localized to small plaques at cellcell interfaces and can be detected throughout early embryogenesis in a pattern suggesting that most or all cells express inx-3. In adults, INX-3 is reduced such that only a few plaques are associated with vulval muscles. In the late L3 stage, INX-3 expression begins in the sex myoblasts (SMs). Expression continues in SM descendants so that all 16 sex muscles stain with anti-INX-3 in early L4 animals, confirming results obtained with an inx-3::gfp translational fusion gene. |
At embryonic 2-cell stage, localized to small plaques at cellcell interfaces. At the late first larval (L1) stage, INX-3 is present transiently in some newly generated cells, and in cells of the first two divisions of the M blast cell, coelomocytes, and sex muscles. INX-3 is readily detectable in the cytoplasm of these cells, as well as in cell-surface plaques. By the comma stage, INX-3 is localized principally in puncta at plasma membranes. At comma stage, within intestinal cells, whose large size allows easy visualization of subcellular location, INX-3 is localized to the basal portion of lateral membranes. |
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early embryo (author) = blastula embryo (curator) --wjc. |
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Expr1736
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In early embryos, MES-3 protein is present in the nuclei of all cells. As embryogenesis progresses, staining gradually diminishes in somatic cells. In late embryos and L1 larvae, MES-3 is detectable in some somatic cells but is most prominent in Z2 and Z3, the primordial germ cells. The nuclear staining of MES-3 is reduced below detection in any of the four nonconditional alleles of mes-3. In wild type adults, MES-3 is most prominent in germline nuclei and is occasionally barely detectable in intestinal nuclei. In the germline, it is present at low levels in distal mitotic nuclei, undetectable in the pachytene region of the distal arm, and present at elevated levels in the proximal meiotic region and in oocytes. |
MES-3 is localized predominantly in nuclei. The immunolocalization pattern of MES-3 was analyzed in embryos, using confocal microscopy. Cells at different stages of mitosis were stained by affinity-purified anti-MES-3 antibody and anti-penta-acetylated H4 antibody to visualize chromosomes. During interphase and prometaphase, when condensed chromosomes are clearly visible in nuclei, MES-3 protein is not obviously concentrated on chromosomes; instead it appears evenly distributed in the nucleoplasm. During metaphase and early anaphase, when nuclear envelopes are broken down, some MES-3 protein is detectably associated with chromosomes. |
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Expr2579
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SCC-1/COH-2 was expressed in germ cells throughout the development, including the adult stage. SCC-1/COH-2 was detected in virtually all mitotic germ nuclei. Similarly to somatic cells in embryos, SCC-1/COH-2 was dispersed in the cytoplasm at mitotic prometaphase and was absent from the condensed anaphase chromosomes in germ cells. In female germ cells that entered meiotic prophase in adult hermaphrodites, SCC-1/COH-2 was observed uniformly in the nuclei. It was unclear whether SCC-1/COH-2 localized to the condensed meiotic chromosomes, because of the strong SCC-1/COH-2 signal emitted from the nucleoplasm. SCC-1/COH-2 was detected also in male germ cells at mitosis and meiosis, but it was not detectable in mature sperm. SCC-1/COH-2 was strongly expressed in virtually all cells in early embryos, but its expression was gradually weakened, and the signal could hardly be detected in late embryos, in which cell division was ceased almost completely. Strong nuclear signals of SCC-1/COH-2 reappeared in larvae, though they were limited to a subset of cells. SCC-1/COH-2 was detectable only in cells that were going to divide. For example, in an L1 larva, intense SCC-1/COH-2 signals were detected in the 14 hypodermal V lineage cells, which divide synchronously. The SCC-1/COH-2 signal was dispersed and not detectable on condensed chromosomes, as observed in embryos of an intermediate stage. In a slightly older L1 larva, expression of SCC-1/COH-2 was seen in 22 P lineage cells to constitute the ventral nerve cord and in four Q lineage cells to produce posterior neuronal cells, all of which divide at the same time. In this L1 larva, no signal was detected in the V lineage cells, suggesting that the SCC-1/COH-2 protein is present only for a short time in the cell cycle, and likely to be degraded quickly after cell division. Larvae of later stages also expressed SCC-1/COH-2 in dividing cells: in an L3 larva, SCC-1/COH-2 was detected in four M lineage cells to produce the uterine and vulval muscle cells and in 10 P lineage vulval precursor cells, which divide concurrently. The embryos were stained with both anti-SCC-1/COH-2 antibodies and an antibody against a component of the nuclear pore complexes. The SCC-1/COH-2 signal was evenly distributed within the nuclear envelope except for the chromosomal region, suggesting that SCC-1/COH-2 molecules dissociated from the chromosomes at metaphase were trapped by the nuclear envelope. Consistently with this interpretation, the SCC-1/COH-2 staining around the metaphase plate was no longer seen at later stages of embryogenesis involving >30 cells, where nuclear envelope is known to break down before metaphase. SCC-1/COH-2 was dispersed into the whole cytoplasm of metaphase cells at these stages. |
SCC-1/COH-2 seemed to localize to the chromosomes in a cell cycle-dependent manner. In interphase, SCC-1/COH-2 was seen throughout the nucleus, overlapping largely with DNA. At mitotic prophase, SCC-1/COH-2 started to separate from condensing chromosomes, and it was not detected on the chromosomes at prometaphase and metaphase. At metaphase, the SCC-1/COH-2 signal seemed as if surrounding the metaphase plate, although it was possible that a small amount of SCC-1/COH-2 was remaining on the metaphase chromosomes but escaped detection, because cohesin is reported to become detectable on metaphase chromosomes only after detergent extraction of soluble background in other metazoans. The SCC-1/COH-2 signal was then dispersed in the cytoplasm at anaphase. At telophase, the SCC-1/COH-2 protein began to reaccumulate on the chromosomes. |
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Picture: Fig. 5. The same pattern was seen with two separate antibodies raised against distinct PLP-1 peptides, and both nuclear and P granule expression was largely eliminated in plp-1 (RNAi) embryos, confirming their specificity. |
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Expr8706
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Immunoreactive PLP-1 localizes to the nuclei of all blastomeres beginning by the two-cell stage of embryogenesis, implying that PLP-1 is a maternally encoded transcription factor. It is also present in the germline-specific P granules of early embryos. |
PLP-1 is transiently asymmetrically localized during telophase of the dividing EMS cell (observed in 12 embryos at the correct stage), with higher levels of the protein in the chromatin of the future E cell nucleus and low or undetectable levels in that of MS. A similar transient asymmetry in PLP-1 levels was observed at many divisions throughout early development, starting at cleavage of the zygote, with higher levels seen in the cytoplasm and forming nucleus of the posterior daughter, P1 (observed in 5 embryos). The anteroposterior asymmetry in PLP-1 was also observed in the AB lineage during the division of the AB granddaughters (observed in 7 embryos): for example, PLP-1 is higher in the chromatin of the posterior daughter ABalp than that of its anterior sister ABala. In all cases, the asymmetry was observed only during telophase and at the time that nuclei were reassembling after cell division; the staining was symmetric at all other times. PLP-1 was always seen at higher levels in the forming nuclei of the posterior daughters. |
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Other strain-- UL123 |
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Expr103
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This strain exhibits strong expression in the embryo. Expression is first seen in the 50-80 cell embryo and extends through to adulthood. It appears that most of the AB cells in the embryo stain, and what appears to be the cells of the C lineage. Some embryos exhibit staining in the two rows of nuclei that are the E lineage. All embryonic staining is very intense, and it spreads to the cytoplasm giving blue embryos, therefore obscuring the DAPI staining, making it difficult to count the number of cells in the embryos as each component begins expressing. This intense staining fades as the embryo ages, sometimes leaving blue comma stage embryos with no distinct nuclei staining. Hypodermal expression is seen in the 3 fold stage of embryogenesis and in young larvae which most probably are C-derived hyp-7 nuclei. Expression weakens as the worm gets older and is much less frequently expressed in adults. Some adults do show staining in the anterior hypodermal nuclei (hyp-3, hyp-4) and in the anterior hypodermal seam cells, also some nuclei stain in the tail. |
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Expr2947
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In late embryos (after the comma stage) matefin staining decreased in all somatic cells but intensified in the nuclear envelopes of the two primordial germ cells, Z2 and Z3. The identity of Z2 and Z3 cells was verified by double labeling with antibodies against PGL-1, which is specific to germ cells. Throughout larva stages L1-L4 and in adults, matefin was present only in germ cells. Matefin signal declined during spermatogenesis and was undetectable in sperm. |
Matefin was detected at the nuclear envelope of all early embryonic cells. |
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sdz-4 = C32B5.16 |
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Expr3146
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Expressed ubiquitously starting at the 12-cell stage. |
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sdz-33 = Y56A3A.14 |
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Expr3147
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Expressed ubiquitously starting at the 12-cell stage. |
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sdz-36 = ZK1251.7 |
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Expr3148
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Expressed ubiquitously starting at the 12-cell stage. |
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This information was extracted from published material (Archana Sharma-Oates, Andrew Mounsey and Ian A. Hope). |
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Expr706
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NHR-2 is detected in the nuclei of embryos as early as 2-cell stage. The protein is present in every nucleus until the 16-20 cell stage then no longer detected in germline precursor P4 and its sister D but at this point expression in other cells increase. No staining during or just after mitosis. 28-cell stage: Staining in E and MS descendants, variable expression generally weak particularly in E cells. Staining in ABplp and ABpr descendants also variable but can be quite strong. The other 10 AB cells and 4 C cells exhibit reproducible strong expression. 51-cell stage: No expression in descendants of E. Staining in C cells, many AB cells and some MS cells (particularly those in anterior and dorsal positions). As embryogenesis progresses NHR-2 expression is restricted to anterior and dorsal regions of embryo. 250 cell stage: Nuclei staining include (but not limited to) Cp descendants contributing to hyp7 synctium, many but not all AB descendants. NHR-2 last detected in one or a few nuclei in vicinity of excretory cell before expression ceases at early comma stage. |
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Expr3279
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In the embryo, the downstream promoter (ten-1b) is most active in the descendants of the ABp cell and in the hypodermis. The dorsal hypodermal cells and the ventral leader cells were most prominently labeled. During postembryonic development, GFP fluorescence was visible in specialized epithelial cells including the arcade cells of the anterior end and the excretory duct. Ten-1b is also active in a subset of neurons including CAN and HSN neurons as well as neurons of the lumbar and retro-vesicular ganglion and some nerve ring interneurons. In males, GFP fluorescence is also visible in R8 and R9 ray neurons. |
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Expr8167
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Expressed in ABalaaxx, ABalpapax, ABalppapx, ABarappx, ABplaapax, ABplapax, ABplpaax, ABplppapx, ABpraapax, ABprapppx, ABprpaax, Abprppapx (97 neurons, 3 hypodermal cells, 1 arcade cell, 17 glia, 2 excretory system cells, 7 postembryonic blast cells). Onset time: 100 to 200 cells. Expressed in descendents of all 16 initial AB descendents with highly patterned expression: Onset time: 50 to 200 cells. |
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In situ hybridization showed that ceh-13 mRNA was not present at early embryonic stages. It appeared first in E.p and then in the AB.xxxp cells, only a short time before CEH-13. Transgenic Marker: rol-6(su1006). Subcellular localization: : Nuclear in E.p, cytoplasmic in AB.xxxp. Nuclear in E.p and Ab.xxxp daughters. In situ hybridization showed that ceh-13 mRNA was not present at early embryonic stages. It appeared first in E.p and then in the AB.xxxp cells, only a short time before CEH-13. Transgenic Marker: rol-6(su1006). |
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Expr513
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Expressed weakly in intestinal precursor, E.p, at 26-cell stage embryo at the beginning of gastrulation. Expressed in E.p and AB.xxxp daughters and in D.a and D.p. See Expression pattern 512 for expression later in development. |
Nuclear in E.p, cytoplasmic in AB.xxxp. Nuclear in E.p and Ab.xxxp daughters. |
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Expr1633
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First, pKK52 expression begins at the 28-cell stage in all four granddaughters and 16 great-great granddaughters of the MS and AB founder cells, respectively; this expression continues in many, possibly all, of their descendants until around the time of hatching. Second, expression becomes more pronounced in seam cells about 1 hour after their birth. This seam expression remains strong throughout embryonic and larval development, but becomes slightly reduced in adults. Third, robust expression is also seen in several cells in the head region, at least some of which are cells in the nervous system (neurons and/or support cells), beginning at approximately the comma stage and continuing through adulthood. For simplicity, this component of the expression pattern was referred as nervous system expression, although the precise identity of these cells were not determined. |
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See Expr1633 for pKK52 expression pattern. |
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Expr1634
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pKK41 is expressed in the same groups of cells as the elt-5 translational reporter (pKK52), but the relative expression levels are different. Whereas the elt-5 reporter is strongly expressed in both seam cells and the nervous system during the comma through pretzel stages, the elt-6 reporter is strongly expressed only in the nervous system. Only weak expression of the elt-6 reporter is apparent in seam cells and in the AB and MS descendants during embryogenesis, but the seam expression becomes stronger during larval development. Strong expression of the elt-6 reporter in the nervous system continues throughout larval development. |
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Removal of the most upstream 1.5-kb HindIII fragment from pMF1 did not affect the expression pattern. The 3.4-kb HindIII fragment (enh3.4) is responsible for a large part of the normal embryonic ceh-13 expression pattern. The 1.2-kb HindIII fragment (enh1.2) is located more proximal to the coding region of pMF1. This fragment appears not to be required for embryonic expression, but drives expression of a GFP reporter gene in larvae and adults, for example, in the male tail. Reporter gene fusion type not specified. The enhancer region of ceh-13 contains different regulatory regions that are responsible for various aspects of the developmental expression pattern of this gene. |
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Expr1771
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pMF1, like the endogenous ceh-13 gene, is first expressed at the onset of gastrulation in the posterior daughters of the intestinal precursor cell E (Ep) and of the AB descendants ABxxx (ABxxxp). During later embryogenesis, CEH-13::GFP is detected in many different tissues and cell types. At the comma stage, for example, it is expressed in the lateral hypodermal cells H2 and V2, in anterior dorsal hypodermal and body wall muscle cells and in cells of the prospective ventral nerve cord (VNC). |
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Feature : "ceh-13.enh3.4" WBsf919526 |
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Expr11275
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The 3.4-kb HindIII fragment is responsible for a large part of the normal embryonic ceh-13 expression pattern. If cloned into pPD107.94, a gfp reporter gene plasmid containing a minimal promoter derived from the pes-10 gene, enh3.4 was able to drive an early embryonic GFP expression pattern indistinguishable from that of the endogenous ceh-13. In comma-stage embryos, enh3.4 recapitulated a large part of the normal ceh-13 expression pattern, including expression in cells of the future VNC and embryonic dorsal hypodermal and body wall muscle cells.However, we also observed some ectopic reporter gene expression in the posterior endoderm and in a few non identified cells of the posterior part of comma-stage embryos. |
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Feature : "ceh-13.enh740" WBsf919528 |
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Expr11276
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The terminal 740 bp (enh740) of enh3.4, when cloned into pPD107.94, were sufficient to initiate the correct early embryonic expression pattern. During the comma stage, however, enh740 failed to induce important aspects of the GFP expression pattern seen with the entire enh3.4. Particularly, GFP expression in embryonic dorsal body wall muscle cells and cells of the future VNC was missing. |
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Expr514
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E.p and daughters during gastrulation, then fades during morphogenesis. No staining seen in larval or adult intestine; AB.xxxp and their daughters during gastrulation; D.a and D.p during gastrulation; unidentified anterior embryonic cells, other cells in AB, MS and D lineages throughout embryogenesis. Strongly expressed in H2L, H2R, V1L, V1R at comma stage embryo. Also seen in anterior dorsal hypodermal cells and anterior body wall muscle cells at comma stage Embryo. Ventral nerve cord, lateral hypodermal and dorsal hypodermal cells show strong expression at L1. H2L and H2R show weak expression at L1. V1.pxx cells do not show expression at L1, but all V1 through V4 descendants show expression at L2. Expressed in male tail at unspecified stage. |
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During all developmental stages, ceh-43::gfp expression resembles the antibody staining pattern published by Panganiban et al. (1997). Therefore, both methods are likely to reflect the natural ceh-43 expression pattern. However, gfp expression is visible generally in fewer cells and is absent from most nerve ring neurons. Therefore, the reporter may not show the complete expression pattern. The short pDllB promoter drives expression only in the main body syncytium, hyp7, where pDllA is not expressed. Authors believe that this expression may not reflect the natural ceh-43::gfp expression, because it is not consistent with the antibody staining from Panganiban et al. (1997). Reporter gene fusion type not specified. |
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Expr1681
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During larval stages, ceh-43::gfp diminishes and is almost absent in adults. In newly hatched larvae, we identified the binucleate dorsal hyp3 and ventral hyp4 cells, the CAN neurons, and the PVQ neurons. Sheath and/or socket cells of several other anterior sensilla are stained as well, identified from their morphology and their position around the pharynx procorpus. In 3-fold stage embryos that move around in the eggshell, the mouth opening can occasionally be seen from above; at the tip of the head, a small ring encircles the mouth opening. It most likely belongs to a small cylindrical hypodermal syncytium such as hyp4 or hyp3, or other small hypodermal cells that connect the buccal cavity to the mouth. All the identified and suspected cells belong to the AB lineage. ceh-43::gfp expression starts around gastrulation in several superficial cells. By following cell divisions, almost all fifth generation descendants of the AB blastomere were identified as GFP positive. Shortly before morphogenesis, GFP expressing cells lie anteriorly, laterally, and anterodorsally at the surface of the embryo. These positions are characteristic for clones of AB descendants. Not all the progeny of the AB blastomere express GFP. At 1.5-fold egg length, most embryonic cell divisions have occurred. At that time, GFP expression is strongest in cells surrounding an indentation at the anterior end, the anterior sensory depression, as well as in two superficial bilateral cells and one ventral cell in the tail. Among these cells are most likely the cells identified in larvae or their precursors. GFP expression is weaker in lateral head regions, the position of future nerve ring neurons. |
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Expr3979
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Broad and dynamic GFP expression was observed in the embryo. GFP expression was seen in the nuclei of the ABplp(a/p), ABalp(a/p), ABprp(a/p), ABara(a/p), and weakly in the ABarp(a/p) blastomeres at approximately 100 min after fertilization. Expression was not seen in the ABpraa. GFP expression was maintained in the progeny of the ABara(a/p) blastomere through the next three cell divisions but was lost in additional blastomeres. In the subsequent cell divisions, GFP expression was maintained in the daughters of the ABaraap precursors which give rise to the NSM(L/R) neurons, but was downregulated in additional ABara(a/p) daughter and grand-daughter cells. GFP expression was weaker in subsequent cell divisions and was not followed further. |
GFP was localized to the nuclei of all expressing cells as expected for a predicted transcription factor. |
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Transgenic lines containing pCZ178 rescued both the uncoordination and cellular defects of the ventral cord motor neurons of cnd-1(ju29) mutants. To minimize misrepresentation caused by the mosaicism of the extrachromosomal arrays, authors collected data from three independent transgenic lines containing pCZ179 or pCZ178 respectively. |
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Expr954
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pCZ178 and pCZ179 were expressed in similar sets of cells, however, GFP expression from pCZ178 was much weaker than from pCZ179 in most cells. CND-1::GFP expression was first detectable in four descendants of the AB lineage of 14 cell embryos. AB derived neuroblasts give rise to most of the C. elegans nervous system. By the 24-cell stage, approximately 75 minutes postfertilization, CND-1::GFP was found in 15 AB derived blastomeres. CND-1::GFP expression was observed in numerous unidentified nuclei throughout gastrulation and epidermal enclosure. By early comma stage, approximately 360 minutes postfertilization, CND-1::GFP was found in many postmitotic neurons in the head and in the ventral cord. The expression of CND-1::GFP in the ventral cord neurons was maintained until hatching, but disappeared completely by the end of the first larval stage. CND-1::GFP was not observed in postembryonically derived motor neurons. To determine whether cnd-1 was expressed in non-neuronal cells of the AB lineage, embryos carrying cnd-1::GFP transgenes were double labeled with anti-GFP and anti-LIN-26 antibodies. In all embryonic stages examined the expression of CND-1::GFP and LIN-26 did not overlap. To confirm the identity of specific AB-derived blastomeres during later stage embryogenesis, embryos carrying CND-1::GFP transgenes were double labeled with anti-GFP and anti-UNC-86 antibodies. CND-1::GFP and UNC-86 are primarily expressed in different subsets of mitotic and postmitotic neurons throughout embryogenesis. At 230 minutes postfertilization, UNC-86 is expressed in ABplaaaaaa, ABarpapaaa, ABplapaaaa, ABprapaaaa, ABarppaaap, and ABarpppapp blastomeres (Finney and Ruvkun, 1990). At the same stage, CND-1::GFP was found in a non-overlapping set of neuroblasts derived from the ABplppap and ABprppap, including ABplppaap, ABplppapp, ABplpppaa, ABprppapa, ABprppaap, ABprppapp and ABprpppaa, which give rise to the embryonic ventral cord motor neurons. In summary, reporter transgene analysis reveals that CND-1::GFP is expressed in both mitotically active neuroblasts throughout embryogenesis, and in subsets of postmitotic neurons including the ventral cord motor neurons. |
Transgenic lines containing pCZ178 show that GFP was localized to the nucleus. |
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Subcellular localization: GLP-1 was found in the cytoplasm at the 2-cell stage, then in cytoplasm and membranes at 4-cell and 8-cell stages. Cytoplasmic GLP-1 fades after the 8-cell stage, and disappears by the 28-cell stage. Membrane-associated GLP-1 is faint by the 28-cell stage. The glp-1 mRNA was distributed uniformly through the 8-cell stage. Levels of glp-1 mRNA decline after the 8-cell stage and largely disappear by the 28-cell stage, though signal consistently persisted later in posterior parts of embryos. mRNA reappears after 100-cell stage, paralleling immunostaining results. early embryo(author) = blastula + gastrulating embryo(curator). |
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Expr541
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Faint expression in AB at 2-cell stage, becoming stronger in AB descendants after 4-cell stage. Signal weakens, between the 8- and 28-cell stages. GLP-1 not detected again until after the 100-cell stage in unidentified cells. |
GLP-1 was found in the cytoplasm at the 2-cell stage, then in cytoplasm and membranes at 4-cell and 8-cell stages. Cytoplasmic GLP-1 fades after the 8-cell stage, and disappears by the 28-cell stage. Membrane-associated GLP-1 is faint by the 28-cell stage. The glp-1 mRNA was distributed uniformly through the 8-cell stage. Levels of glp-1 mRNA decline after the 8-cell stage and largely disappear by the 28-cell stage, though signal consistently persisted later in posterior parts of embryos. mRNA reappears after 100-cell stage, paralleling immunostaining results. |
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Reporter gene fusion type not specified. |
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Expr1601
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Expressed on the surface of motile cells and pioneering neurons whose migrations are affected in unc-40 mutants. UNC-40/GFP becomes detectable on the surface of all cells at the onset of gastrulation (~100 min after first cleavage), and then gradually decreases. By the end of gastrulation (~290 min), the protein is barely detectable on all cells. In the neurula (~400 min), UNC-40/GFP is highly expressed on ventral cord motorneurons, including cell bodies and axons, undergoing axonogenesis. Additional neurons express UNC-40/GFP soon after, but are difficult to identify in the elongating neurula. This expression generally persists into the first larval stage and beyond, allowing unambiguous identification of most cells. Similar expression patterns were observed using unc-40 upstream regulatory sequences to direct cytoplasmic expression of soluble GFP. In first stage larvae, ventral epidermoblasts P1/2 to P11/12 (Pn cells) express UNC-40/GFP as they undergo planar movements within the epithelium. Similarly, neuroblasts QL and QR and their descendants express UNC-40/GFP as they migrate longitudinally along the epidermis. In second stage and later larvae, the distal tip cells of hermaphrodites express UNC-40/GFP as they migrate along the body wall. |
cytoplasmic expression |
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This information was extracted from published material (Archana Sharma-Oates, Andrew Mounsey and Ian A. Hope). |
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Expr705
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Pattern very similar to NHR-2 protein. Fusion protein is not seen prior to 16-cell stage. At the 16 to 20-cell stage all cells express except P4 and D. Expression becomes restricted mirroring that for NHR-2 and is ultimately observed in 2-4 cells in head region before disappearing entirely by early comma stage. NHR-2/beta-gal immunostained with anti-beta-gal Ab. 24-cell stage every nuclei stained except P4 and D. 50-cell: many posterior, internal cells do not stain. 500 cell stage 3 cells in presumptive head region stain. X-gal staining same as above. |
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