|
|
|
Expr4287
|
psa-3 was expressed in the T cell, head neurons, posterior gut cells, hypodermal cells (hyp7, hyp9, and hyp10), and P blast cells. Of the seam cells, only the T cell expressed psa-3. During mitosis of the T cell, the PSA-3 protein was uniformly distributed in the T cell. Soon after the T cell division (before V6 cell division, which occurs about 30 min after T cell division), the psa-3 expression in the two daughter cells was almost the same. In the later stage, after V6 cell division, the psa-3 expression in T.a had decreased and that in T.p increased. After the next round of divisions, the psa-3 expression had greatly increased in the posterior (T.pa and T.pp), but not the anterior, granddaughters. |
|
|
mhIs9 rescued the lin-17 T and B cell polarity defects. |
|
Expr4251
|
mhIs9 males contain a lin-17::gfp construct that was expressed in the membranes of the T, B cells and their descendants as well as the F, P11, P12 and vuval precursor cells. |
membrane |
|
New Anatomy_term: male hook precursors (L1-L4). Picture: Figure S3A. |
|
Marker87
|
Marker for VPC daughters and granddaughters. Expressed in P cells (L1), QL and QR cells (L1-L2), somatic gonadal precursor (L1), V cells (L1), B cell (L1), T cell (L1), ventral cord neurons (L1-L4), Pn.ps (L1-late L2), Pn.pxx (mid L3), male hook precursors (L1-L4), DTCs (L2-L3), vulval cells (L3-L4), uterine cells (L4), vulval muscle (adult), many unidentified cells in head (all), many unidentified cells in tail (all) |
|
|
|
|
Expr886
|
The levels of POP-1 were higher in the anterior T cell daughter in wild-type animals(28/28). In lin-17 animals, which display a loss of T cell polarity, the level of POP-1 was high in both T cell daughters in 71% of divisions, higher in the posterior T cell daughter in 8% of divisions and higher in the anterior T cell daughter in 17% of divisions (n=65). |
|
|
This information was extracted from published material (Archana Sharma-Oates, Andrew Mounsey and Ian A. Hope). |
|
Expr660
|
9h after fertilization: strong staining in intestinal and hypodermal nuclei; Weak neuronal staining. Early L1: staining in nuclei of most postembryonic blast cells. Strong staining in nuclei of hypodermic blast cells H1, H2, V1-V6, T and all intestinal (E) cells. Weak staining nuclei of neuroblasts Q1 and Q2, mesoblast M cells and P cells. 9h after fertilization: strong staining in intestinal and hypodermal nuclei; Weak neuronal staining. Early L1: staining in nuclei of most postembryonic blast cells. Strong staining in nuclei of hypodermic blast cells H1, H2, V1-V6, T and all intestinal (E) cells. weak staining nuclei of neuroblasts Q1 and Q2, mesoblast M cells and P cells. Adult: staining observed in the mature oocyte nuclei of hermaphrodites, at meiotic prophase I when the chromosomes are condensed. (Possible artifact, detected in lin-14 loss-of-function mutant strains n536n540, n355n726). In embryo, first observed in embryo at 7h after fertilization (half way through embryogenesis). Strong staining in intestinal and hypodermal nuclei. L3: Pn.p stains weakly before division (staining fades by L4). Occasional weak staining of hypodermal, intestinal and neuronal nuclei and cytoplasm at L2 and L3. Late L1: staining of all nuclei except for neuronal nuclei is weaker. More neuron of the nerve ring and posterior ganglion stain than in earlier stages. Intestinal and hypodermal cell lineages stain strongest at mid to late L1 (Fade entirely by L2) similarly with many of the neuronal cells. Mid L1: staining in nuclei of hypodermic blast cells H1, H2, V1-V6 and T. The nuclei of intestinal (E) cells also stain. Weak staining in nuclei of P cells (staining fades before migration into ventral cord). Strong staining in nuclei of embryo-derived nuclei in hypodermal syncytial cell hyp7, ABarpppapa, ABplaapppp, Cpaaaa, Cpaapa, Cpaapp, Cpapaa, terminally differentiated nuclei from embryonic body muscle also stain for lin-14. Staining observed in nuclei of neuronal cells BDU, ALM, and CAN. All embryonic generated ventral cord neurons and some neurons of the nerve ring and posterior ganglion stain for lin-14. |
lin-14 is localized to the nuclei. |
|
Lineage expression: H, V, T descandents. This information was extracted from published material (Archana Sharma-Oates, Andrew Mounsey and Ian A. Hope). |
|
Expr661
|
lin-14 protein is first observed in embryos at ~7 hours after fertilization where most intense staining is seen in intestinal and hypodermal nuclei. ~9 h after fertilization, additional weak staining is observed. lin-14 protein is expressed at high level in the nuclei of most of the post-embryonic blast cells. Intense nuclear staining was observed in the hypodermal blast cells H1, H2, V1-V6 and T and in all of the intestinal (E) cells and weaker staining was observed in both neuroblasts Q1 and Q2, in the mesoblast M cell and in P cells (P1/2, P3/4 and P5/6). During L1, staining is seen in the progeny of the hypodermal blast cells H1, H2 V1-V6 and T and in all of the intestinal (E) cells. Staining in P-cell nuclei fades before migration into the ventral nerve cord but reappears later in some of their progeny cells. The embryo-derived nuclei in the hypodermal syncytial cell hyp7, ABarpppapa, ABplaapppp, Cpaaaa, Cpaapa, Cpaapp, Cpapaa, all stain for the lin-14 protein during the L1 stage. Terminally differentiated nuclei from embryonic body muscle also accumulate the lin-14 protein. Nuclei of many but not all neuronal cells stain with the antibody (e.g. BDU, ALM, CAN but not HSN). All of the embryonically generated ventral cord neurons and some but not all of the neurons of the nerve ring and the posterior ganglion accumulate the lin-14 protein in their nuclei during the L1 stage. Late L1 stage, staining is seen in all nuclei except in the neuronal nuclei staining is much weaker. In addition, more neurons of the nerve ring and posterior ganglion stain than at the earlier stages. Thus, in the hypodermal and intestinal cell lineages, lin-14 protein level peaks during early L1 and fade entirely by L2. In the many neuronal cells, lin-14 protein peak during mid to late L1 and fade by L2. Pn.p accumulates lin-14 protein at the L3 stage, although, very weak staining is seen before the Pn.p cells divide. This staining fades by early L4, In occasional L2 and L3 stage animals, weak staining is observed in nuclei and cytoplasm of hypodermal, neuronal and intestinal cells. Patches of staining in hypodermal or intestinal nuclei is only rarely observed in very old adults. In most adults, staining reappears only in the mature oocyte nuclei of hermaphrodites at meiotic prophase I when the chromosomes are condensed. The oocyte nuclear staining disappears after fertilization. Quantitation of immunoblots show that the level of lin-14 protein relative to a pharyngeal myosin control decreases >= 25-fold from L1 to L2. |
|
|
This information was extracted from published material (Archana Sharma-Oates, Andrew Mounsey and Ian A. Hope). |
|
Expr709
|
Expression first detected in embryos though to adulthood. In L1, strong staining detected in the pharynx and in 2 laterally located cells (NLS-lacZ staining). The pharyngeal cells are muscle cells which occupy most of the body of the pharynx and the lateral cells were CAN neurons based on the position of the nucleus and axon morphology. Both pharyngeal muscle and CAN neurons express reporter as embryo through to adulthood. Also stained were several cells in the tail region. These include the B and Y cells (forming male spicule) from L1 to adult, the hypodermal blast cells T in the L1 and some of its progeny in later stages. In L1, subset of cells in ventral nerve cord and DA identified as DB neurons (cholinergic motor neurons innervating dorsal body wall muscles) stain. Cells identified by GFP: GFP without NLS revealed expression in distal tip cells (DTC) spermatheca and uterus. It is not clear if GFP is expressed by somatic cells of the gonad or by the germline cells (namely sperm) in the spermatheca. Expression in uterus was seen outside the embryos. It is not clear which cells expressed the reporter in uterus although observation of NLS-lacZ and NLS-GFP indicated that some somatic cells of the gonad expressed CePAKGFP without NLS. There is expression in many hypodermal cells surrounding the embryos during the morphogenetic stage. C-terminus two amino-acids of CePAK replaced with GFP coding sequence and fusion protein was expressed from the CePAK promoter used to analyze intracellular localization (pCPK2.77). CePAK GFP was enriched at cell surface in pharyngeal muscle cells especially condensed at cell boundaries. In CAN neurons CePAK GFP detected in cell bodies and along the axons. CePAK GFP localized to cell bodies and their processes running along the excretory canal on the lateral surface of adults. |
|
|
Interestingly, Y is replaced in the hindgut by P12.pa, a descendant of the only P cell in which PEB-1 protein expression was detected in L1 larvae. No detailed description on cellular expression patterns in pharynx, try to find those information in Expr838. |
|
Expr3462
|
In summary, PEB-1 accumulated in L1 larvae in the nuclei of all hypodermal cells and the epithelial cells lining the rectal lumen. As in the pharynx, PEB-1 was not detectable in neuroblasts or differentiated neurons. PEB-1-expressing cells are not obviously related by cell type or lineage. Rather, one striking common feature of these cells is that they contact the cuticle on the exterior of the worm or lining the pharyngeal or rectal lumen. Like in the pharynx, PEB-1 was first detected in the hypodermal nuclei in comma stage embryos (approximately 400 min) and remained detectable until hatching. In 1 1/2-fold stage embryos, the PEB-1 protein was detected in the nuclei of most, if not all, hypodermal cells including hyp5, hyp6, and hyp7 and the H, P, and V cells. After hatching, PEB-1 remained detectable in most hypodermal cells although it decreased in later larvae and was undetectable in adults. In the L1 lateral hypodermis, the PEB-1 protein was detected in H0, H1, H2, V1 to V6, and T, and their anterior and posterior daughters, as well as in the nuclei of the hyp7 syncytium. PEB-1 was also detected in many of the dorsal and ventral hypodermal nuclei in the head and the ventral hypodermal nuclei in the tail. Notably, PEB-1 was not detected in larval P cells. In addition, PEB-1 was not detected in other neuroblasts including Q and T.p. PEB-1 was also expressed in cells lining the lumen of the hindgut. In 1 1/2-fold embryos (approximately 420 min), PEB-1 was detected in many nuclei near the posterior of the embryo. These likely include both the posterior hypodermal cells and hindgut cells, although these cells cannot be easily distinguished at this stage. In L1 larvae, PEB-1 was detected in many of the non-neuronal nuclei surrounding the rectal lumen, including K, K', U, F, B, and Y. PEB-1 was not detected in the rectal-intestinal valve or the anal depressor muscle. As in other tissues, the PEB-1 protein remained detectable in the hindgut throughout larval development but became progressively less abundant and undetectable in adults. Importantly, this progressive decrease in PEB-1 expression also occurs in Y, which withdraws from the hypodermis during late larval development to become a neuron. |
nuclei |
|
Reporter gene fusion type not specified. |
|
Expr1614
|
At the beginning of embryonic morphogenesis, all ten pairs of lateral epidermal cells, the seam cells, express cdh-3::lacZ. cdh-3::GFP expression in these cells is observed at hatching and throughout subsequent postembryonic development. During the last larval stage (L4) the 15 pairs of seam cells generated during larval development fuse to form two continuous lateral syncytia, surrounded by hyp7. cdh-3::GFP expression correlates with seam cell identity during these postembryonic divisions; it is not observed in daughters that fuse with hyp7 or adopt other fates. In embryos undergoing morphogenesis, lacZ is expressed in a single large nucleus, whose size and position is consistent with that of the excretory cell. This identification is reinforced by the observation that in many newly hatched L1 larvae, low levels of GFP expression are visible in the excretory cell. This expression of cdh-3-reporter genes was observed only during late embryogenesis and in some newly hatched L1s (the latter may be due to perdurance of the GFP fusion protein), but not at later stages. Several other cells expressed the cdh-3 reporter constructs during embryonic morphogenesis; as in the seam cells this expression continued upon hatching. In the tail two cells, hyp10 and hyp11, show strong GFP expression that persists only during the first larval stage. Strong expression was observed in cells that form interfacial epithelia between the intestinal epithelium and the epidermis. Two cells that form part of the rectal epithelium, designated F and U, express cdh-3::GFP during embryonic morphogenesis and throughout larval development. In the anterior of embryos undergoing morphogenesis there were several cells expressing cdh-3::lacZ, and in larvae and adults, GFP expression is seen in nine cell bodies located just anterior to the first bulb of the pharynx. Processes extend anteriorly from these cell bodies and terminate at the level of the buccal capsule. Based upon the location of the cell bodies and the morphology of the processes, these cells were identified as the anterior and posterior arcade cells. Expression pattern of the pJP#38 construct in males indicated expression in the male tail and several male-specific neurons, however the expression pattern is complicated and the cell identity were not determined. cdh-3::GFP expressed in the developing hermaphrodite vulva. GFP first expressed in the anchor cell in L3 larvae. A little later expression were seen in those vulval cells that are closest to the anchor cell and are beginning to invaginate. As vulval morphogenesis continues all of the cells that invaginate to form the vulva are expressing GFP. During this period, the uterine epithelium closest to the invaginating vulval cells begins to express cdh-3::GFP and the anchor cell fuses with the multinucleate uterine seam cell (utse), which also begins to express cdh-3::GFP. Expression continues in these cells into the adult stage, though at somewhat reduced levels, which may perhaps be due to perdurance of the fusion protein, since older adults show much reduced fluorescence compared with younger ones. During the time that the vulva is forming, cdh-3::GFP expressed in the six VC neurons located in the ventral nerve cord and the two HSNs located just posterior and dorsal to the developing vulva. These cells begin to extend processes at about this time, and GFP expression continues in these cells and their processes throughout the remainder of larval development and into adulthood. |
|
|
|
|
Expr1853
|
During larval development, tlp-1::gfp expressed in the posterior intestinal cells, several neuronal nuclei in the head, the tail tip cells in hermaphrodites and males and in descendants of the T cell lineage. Weak GFP expression observed in the T cell in 6% (n=124) of animals. After the division of the T cell, stronger GFP expression was observed in the posterior T cell daughter, T.p. but not in T.a. More specifically, of the animals that showed GFP expression in the T cell lineage (57/150), 88% of the animals examined showed GFP expression in T.p alone and 12% showed expression in T.a and T.p. GFP expression was also observed in the posterior T.ap daughter cell, T.app but not in T.ap or its anterior daughter cell T.apa. Specifically, all of the animals that showed expression in the T.ap lineage (11/56) showed GFP expression in T.app alone. No expression observed in T.apa in any animals. tlp-1::gfp expression begins to be barely detectable at the beginning of gastrulation at about 100 minutes of embryonic development. Shortly after the gastrulation begins, the level of expression increases and is detectable in the nuclei of most embryonic cells. This pattern appears to persist through gastrulation. However, at about 260 minutes, expression in the anterior of the embryo fades and expression in the posterior of the embryo persists and gets stronger. At the 1.5-fold stage, at about 400 minutes, expression was observed in posterior nuclei and this pattern continues throughout the rest of development. |
nuclei |
|
|
|
Expr2347
|
CYE-1 is present in adult animals and is restricted to the germline, which is the only proliferative tissue in adults. CYE-1 levels vary in the germline. Mitotic germ cells in the distal region of the gonad have easily detectable levels of nuclear CYE-1. Germ cells in the initial stages of meiosis (proximal to the mitotic germ cells) have lower CYE-1 levels. Finally, as oocytes cellularize in the loop region of the gonad, CYE-1 levels increase with mature oocytes having the highest levels of nuclear CYE-1. These results demonstrate that a significant portion of maternal cye-1 contribution to the embryo is CYE-1 protein. CYE-1 level was assayed postembryonically to determine whether CYE-1 could be detected and if levels of CYE-1 correlated with mitotic proliferation. CYE-1 protein is detectable in larval blast cells that give rise to all tissue types, including, germline, intestine, hypodermis, neurons, and muscle. During larval stages, the level of CYE-1 protein is much lower than that found in germ cells or in the early embryo. CYE-1 antibody staining is restricted to the developmental time when the blast cells are undergoing active proliferation. For example, in the L1 stage, proliferating P blast cells that produce ventral nerve cells have relatively high levels of nuclear CYE-1. In contrast, during the L2 larval stage, the nonproliferating neuronal descendents of the P blast cells have CYE-1 levels that are only barely detectable above background. Further, while a subset of the P cell descendents, the vulva precursor cells (VPCs), will proliferate in the L3 larval stage to produce the vulva, these cells do not have appreciable CYE-1 levels while they are quiescent in the L2 larval stage. Nuclear CYE-1 becomes detectable in the VPCs during the L3 larval stage when they begin proliferation. CYE-1 becomes undetectable in the VPC descendents after completion of cell divisions in L4 larval stage animals. Monoclonal anti-CYE-1 antibody was used to assay CYE-1 levels from fertilization to the end of embryogenesis. In the zygote, CYE-1 is observed in the maternal and paternal pronuclei as soon as they form. The specificity of antibody staining was confirmed by cye-1 RNAi treatment of adult hermaphrodites that abolishes both oocyte nuclei and embryonic anti-CYE-1 protein staining. In early embryos, CYE-1 is enriched in nuclei, and levels appear constant with no evidence of cell cycle fluctuations other than during mitosis. During mitosis, CYE-1 antibody staining appears diffuse once nuclear envelope breakdown occurs, but resumes nuclear localization upon reformation of the nuclear envelope in telophase. CYE-1 is present equally in all cells of the early embryo. The level of CYE-1 declines during embryogenesis and disappears from most cells in comma-stage embryos coincident with the completion of the majority of embryonic cell divisions. |
nuclear |
|
|
|
Expr11007
|
egl-18 is asymmetrically expressed in larval seam division daughters with stronger expression in the posterior seam-fated cells in which the Wnt pathway is activated. All ten seam cells in newly hatched L1 larvae showed strong egl-18 expression. After their first division, egl-18::mCherry expression was asymmetric between the daughters, with stronger expression in the posterior daughters that maintain the seam cell fate. Expression in the anterior daughter faded after division, before the hypodermal daughters moved out of the seam cell line. During the L2 stage, several seam cells undergo a symmetric expansion division, generating two seam daughters and increasing the seam cell number from 10 to 16 (Sulston and Horvitz, 1977). In the early L2, strong symmetric expression of egl-18::mCherry was seen in both seam-fated daughters of these divisions. When these seam-fated daughters underwent their subsequent L2 and L3 stage asymmetric divisions, reporter expression faded in their anterior, hypodermal-fated daughters as observed in the L1 stage. In the adult, differentiated seam cells continue to show strong expression of the egl-18::mCherry reporter as described previously (Budovskaya et al., 2008). |
|
|
Other strains-- UL889, UL890 |
|
Expr2004
|
Expression is seen predominantly in embryos (from the precomma stage through morphogenesis) and young larvae, although occasional expression is seen in older larvae and adults. At the 1.5 fold embryonic stage 10 cells running along each lateral side of the embryo can be seen, and are V1, V2, V3, V4, V5, V6, H0, H1, H2, and T. In young larvae expression in the hypodermal seam cells can be seen. |
|
|
early + mid embryo(author) = gastrulating + enclosing embryo(curator). |
|
Expr585
|
At the 200-cell stage, four posterior ventral cells stain, AB.p(r/)lpppp(a/p). At about 350 cells, their eight descendants, and about 12 other cells including lateral and ventral epidermal blast cells, show expression. By the 1.5-fold stage, additional cells stain, e.g., posterior ventral cord neuronal precursors. Most of the cells continue to stain at L1, with the notable exception of the eight descendants of the four cells that show initial staining. |
Muscle sarcomeres and nuclear localization. Staining is nuclear localized. |
|
|
|
Expr10214
|
Inferred expression. EPIC dataset. http://epic.gs.washington.edu/ Large-scale cellular resolution compendium of gene expression dynamics throughout development. This reporter was inferred to be expressing in this cell or one of its embryonic progenitor cells as described below. To generate a compact description of which cells express a particular reporter irrespective of time, the authors defined a metric "peak expression" for each of the 671 terminal ("leaf") cells born during embryogenesis. For each of these cells, the peak expression is the maximal reporter intensity observed in that cell or any of its ancestors; this has the effect of transposing earlier expression forward in time to the terminal set of cells. This metric allows straightforward comparisons of genes' cellular and lineal expression overlap, even when the expression occurs with different timing and despite differences in the precise time point that curation ended in different movies, at the cost of ignoring the temporal dynamics of expression, a topic that requires separate treatment. For simplicity, the authors use the term "expressing cells" to mean the number of leaf cells (of 671) with peak expression greater than background (2000 intensity units) and at least 10% of the maximum expression in that embryo. Quantitative expression data for all cells are located here: ftp://caltech.wormbase.org/pub/wormbase/datasets-published/murray2012/ |
|
|
|
|
Expr3466
|
Expression is most robust throughout embryonic development from 250 minutes after the first cleavage until the early 3-fold stage. Expression was observed in the nuclei of hyp5, H0-H2, V1-V6 and T. Additional ceh-16::gfp expression was also observed in cells of the AB lineage at stages prior to the one described above (28-56 cell stage). These cells were determined in 100 minute embryos as being ABprap, ABarpp, ABpraa, ABplap, ABplaa, ABarpa and ABaraa. In later embryonic stages expression was observed in anterior neurons and in the DA1 and DD1 motoneurons after hatching. |
|
|
|
This construct rescued the tcl-2 T cell and gonad defects, but only partially rescued the Pv1 defects. |
Expr2550
|
tcl-2::gfp is expressed strongly in the cytoplasm of the pharynx muscle cells and several head neurons, probably the IL1s or IL2s, throughout development. Several other unidentified neurons in the tail region expressed GFP throughout development. Although tcl-2 mutants display gonad, and P12.p cell fate defects, GFP expression was not observed in these cells or their descendants in L1 animals. |
In contrast to the cytoplasmic expression in head neurons, weak GFP expression was observed in the nuclei of the T cells and the T cell daughters, T.a and T.p. The level of GFP expression was equal in both T cell daughters. |
|
|
|
Expr11089
|
ceh-20 was expressed in nearly all of the cells, including the T cell. During T cell mitosis, CEH-20 was distributed uniformly. Soon after T cell division (before V6 division), the nuclear level of CEH-20 was equal in the daughter cells, while in the late stage, after V6 division, the nuclear level in T.a was slightly greater and that in T.p was slightly less, resulting in the differential subcellular localization of CEH-20 between the daughter cells (8/33 animals showed the asymmetric localization; i.e., strong nuclear localization in T.a and weak nuclear and cytoplasmic localization in T.p). |
|
|
|
|
Expr3488
|
Expressed in most cells during embryogenesis and in many if not all cells in developing larvae. Expressed in the T cell and the T-cell daughters. GFP fluorescence was observed in both of the daughter nuclei, indicating that there was no asymmetry in the expression pattern of let-19 during T-cell division. |
|
|
|
|
Expr3489
|
Expressed in most cells during embryogenesis and in many if not all cells in developing larvae. Expressed in the T cell and the T-cell daughters. GFP fluorescence was observed in both of the daughter nuclei, indicating that there was no asymmetry in the expression pattern of dpy-22 during T-cell division. |
|
