Picture: Fig. 7. |
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Expr4376
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ceGAT-1 is expressed in all of the GABA-ergic neurons. These GFP-positive neurons include the VD and DD neurons in the ventral cord, the RMED, RMEV, RMEL, RMER, AVL, and RIS neurons in the head area and the DVB neuron in the tail region. There are two additional GFP-positive neurons in the tail region. These two neurons are PVQR and PVQL. The identity of these GFP-positive neurons were confirmed by epifluorescence microscopy and by the location of the neurons as revealed by a combination of Nomarski-differential interference contrast microscopic observation and 4',6-diamidino-2-phenylindole nuclei-staining method. This expression pattern is evident from the early larva stage through the adult stage. An identical expression pattern was observed with at least 10 transgenic animals. |
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Expr15649
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Picture: N.A. Reporter gene fusion type not specified. |
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Marker57
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Expressed in AVL neuron. |
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Expr15558
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Expr9325
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Synaptogyrin is expressed in all 26 GABAergic neurons including also RMER and most though not all other neurons. Synaptogyrin is absent in amphids and phasmids and can be detected in non-neuronal glial-like sheath cells in adult worms. The cephalic neurons CEPDR/L and CEPVR/L and amphid-associated sheath cells CEPshDR/L, CEPshVR/L were tentatively positive. Several other neurons that could be tentatively identified in the anterior part are MI, M4, I4, AVL, AIY, RIS, I5, M3R/L, and in the posterior part DVA, AS11, ALNR/L, DVC, DVB, PQR, DA9 (characteristic axonal process denoted by arrowhead), VD13, DD6, VD12. Of these, AVL, RIS, VD13, DD6 and VD12 are GABAergic based on the colocalization with the unc-47p::GFP reporter. In addition, IL neurons were tentatively identified in the anterior (IL*). Synaptogyrin reporter constructs are also expressed in developing neurons. The expression of sng-1p::YFP is closely associated with the development of the nervous system being absent in the gastrula stage with first fluorescence in neuronal precursor cells and newly-formed neurons in the anterior part during the 1.5-fold stage. In addition, it is also detected transiently in cells in the posterior body at the 1.25-fold and 1.5-fold stage. |
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Expr15571
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Expr15572
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Expr15573
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Expr15579
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Expr15586
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Expr15651
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Expr15652
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Expr15589
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Expr13158
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Expr15591
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Expr15598
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Expr15604
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Expr15608
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Expr15611
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Expr14034
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ADL (dim), AVL, RIS, head mesodermal cell, pharynx (dim), pharyngeal-intestinal valve (dim), anal depressor muscle, stomatointestinal muscle, PVT, DVA, distal tip cell, CAN |
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In snf-11(ok156) mutants, anti-SNF-11 staining was completely absent, confirming the specificity of the staining. Picture: Fig 4. |
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Expr7836
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In healthy young adults, the anti-SNF-11 antibody strongly stained the four RME neurons (RMED, RMEV, RMEL, and RMER). Faint staining of three additional GABAergic neurons (AVL, DVB, and RIS) was sometimes observed. Several non-GABAergic neurons, including RID, also seemed to stain. The ventral nerve cord DD and VD inhibitory motor neurons did not stain. Faint staining of the body wall, anal, and uterine muscles with the anti-SNF-11 antibody was observed in some animals. |
Staining of both the processes and the soma of each neuron were observed. In RMED and RMEV, a punctate staining pattern was observed in the posteriorly directed processes, possibly corresponding to synapses. |
Picture: Figure 5 and Table 1. |
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Expr7837
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These Psnf-11::GFP fusions are expressed in the same neurons (RMEs, AVL, DVB, RIS, and RID) that stained with the anti-SNF-11 polyclonal antibodies. Expression was also noted in two additional neurons near the pharynx as well as two neurons in the retrovesicular ganglion. There were no apparent differences in expression between the two reporters, suggesting that the 1.9-kb region is sufficient to drive expression in all snf-11 positive cells. In contrast to observations reported previously (Jiang et al., 2005 blue right-pointing triangle), authors did not observe snf-11 expression in the ventral cord inhibitory (DD and VD) motor neurons. However, they did observe robust expression in the body wall, anal, and uterine muscles that was not noted previously. In young animals, expression of the Psnf-11::GFP reporter in muscle cells is the most prominent aspect of the expression pattern. |
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Expr15364
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Picture: Fig 6. |
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Expr8786
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Apart from cells in the neuroblast lineage that generate ASE, nhr-67::mCherry was expressed in multiple other neuroblast lineages in the developing embryo. Expression was usually observed in the grandmother or mother of a neuron, but not earlier. Within the ASEL and ASER-generating lineage branches, nhr-67 was expressed in neuroblasts that generate closely or distantly related cousins of ASEL and ASER. For example, the sister neuroblast of the ASE-generating neuroblast creates the AUA and ASJ neurons and it expressed nhr-67. The cousin of the ASE-mother cell generates the AWB and ADF sensory neurons. nhr-67 was expressed in these cells. In late stage embryos, a few other, postmitotic neurons started to express nhr-67. Embryonic nhr-67 expression was not restricted to the nervous system, but was observed in a small subset of mesodermal and hypodermal cells. No expression was detected in endodermal cells or the germ line. nhr-67 was expressed in the excretory canal cell. Postembryonically, nhr-67 expression persisted only in a few neurons in the head ganglia until the first larval stage and faded shortly thereafter in most, but not all, of these neurons, with expression persisting through adulthood only in the CEPD/V, RMED/V, AVL and RIS neurons. During mid-larval development, nhr-67 was transiently and dynamically expressed in the AC cells of the vulva. Expression was also found in the VU cells and somatic gonad, but not in vulA, vulB or vulC. Within the ASEL/R generating lineages, nhr-67::mCherry was first observed in the grandmother cells of ASEL and ASER. Transgenic animals that co-express a functional nhr-67::mCherry reporter and a functional che-1::yfp reporter revealed that nhr-67 precedes che-1 expression. nhr-67 expression was maintained in the ASEL and ASER neurons until the first larval stage after which it became undetectable, whereas che-1 expression was maintained throughout the life of the animal. In spite of its genetically deduced role in asymmetric gene expression in ASEL and ASER, nhr-67 expression is bilaterally symmetric in ASEL and ASER. |
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Reporter gene fusion type not specified. |
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Expr3687
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Hermaphrodites carrying DOP-4::gfp showed GFP expression in pharyngeal neurons I1 and I2, neurons ASG, AVL, CAN, and PQR, vulva, intestine, rectal glands, and rectal epithelial cells. There was also weak and variable expression in several neurons in the head region. Males also showed expression in neurons in ray 8 |
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Expr3021
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Expressed in AIM, ASG, AVA, AVG, AVL, CEP, PVD, PVW, RIC/AIZ, RIV, SMD, URA, uv1. Male specific expression in 6 out of 9 CP. |
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Expr15390
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Expr13957
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Using a fosmid-based GFP translational fusion, we found that zag-1 was expressed in the six TRNs but not in the FLP and PVD neurons. In addition to TRNs, zag-1 was expressed in the AIB, AIM, AIN, AIZ, AVA, AVB, AVD, AVE, AVG, AVK, AVL, M4, M5, RIA, RIB, RIF, RIG, RIM, RIV, RMD, RME, RMF, RMH, SIA, and SMD neurons in the head, all the DD, VD, and VC neurons in the ventral cord, and the DVA, DVB, LUA, PDA, PVC, PVP, PVQ, PVR, and PVT neurons in the tail. zag-1 is also expressed in the serotonergic HSN neurons. |
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Expr15366
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Expr16009
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We found that ckr-1 is broadly expressed in the nervous system, showing expression in a subset of ventral nerve cord motor neurons, amphid and phasmid sensory neurons, premotor interneurons, and motor neurons in the nerve ring. We identified many of these neurons, largely from analysis of ckr-1 co-expression with previously characterized reporters. In the ventral nerve cord, we found that ckr-1 is expressed in cholinergic, but not GABAergic, ventral cord motor neurons. Amongst head neurons, the ckr-1 reporter is expressed in GABAergic RMEV, RMED, AVL and RIS neurons, cholinergic SMDV, SMDD, and RIV head motor neurons, the interneuron RIG, the serotonergic NSM neuron, and in the interneurons AIA and AIB. Additional studies using DiI uptake indicated that ckr-1 is also expressed in the amphid sensory neurons ASK and ASI and the phasmid sensory neurons PHA and PHB. With the exception of the ventral cord cholinergic neurons, the ckr-1 reporter almost exclusively labeled neurons that do not receive direct synaptic input from DVA, suggesting that NLP-12 acts at least partially through extrasynaptic mechanisms. |
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