ライフサイエンスコーパス: seam cell

1 d elt-6 as Wnt pathway targets in the larval seam cells.

2 as it is virtually undetectable in nonfusing seam cells.

3 uences necessary for expression in vulval or seam cells.

4 expression in the developing vulva and adult seam cells.

5 elopment of the lateral epidermal cells, the seam cells.

6 and -6 repress elt-3 expression in wild-type seam cells.

7 ts attachment to the vulva and the epidermal seam cells.

8 or the terminal differentiation of epidermal seam cells.

9 ufficient to redirect the PVD dendrites onto seam cells.

10 Two deficiencies result in multinucleate seam cells.

11 of the three major epidermal cell types, the seam cells.

12 on of the stem cell-like lateral hypodermal (seam) cells.

13 essed exclusively in the lateral hypodermal (seam) cells.

14 inactivate the LIN-28 pluripotency factor in seam cells, a stem-like cell type in Caenorhabditis eleg

15 ired in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva f

16 the anchor cell does not fuse to the uterine seam cell and, instead, remains at the apex of the vulva

17 ectopic Ptbx-2::gfp expression in hypodermal seam cells and gut.

18 elt-5 and -6 are both expressed in seam cells and many other cells, and are apparently func

19 he major hypodermal cells except the lateral seam cells, and expression is initiated immediately afte

20 2 is expressed in the posterior gut, cuticle seam cells, and spermatheca, the first two of which are

21 The C. elegans seam cells are lateral epithelial cells arrayed in a sin

22 Furthermore, because seam cells as well as pharyngeal cells secrete their gly

23 ditis elegans epidermal stem cells, known as seam cells, as a readout.

24 We show that in larval seam cell asymmetric divisions, EGL-18 is expressed stro

25 r level of let-7 gfp transgene expression in seam cells at L3 stage.

26 (DTC), intestine, and the lateral hypodermal seam cells but not in the main body hypodermal syncytium

27 nic mutations that enhance LIT-1 activity in seam cells can simultaneously also enhance the opposing,

28 coordinate development of the vulval-uterine-seam cell connection.

29 ell must fuse with the multinucleate uterine seam cell, derived from uterine cells that adopt a (pi)

30 protein that is required for proper uterine seam cell development in Caenorhabditis elegans.

31 coding GATA factors essential for viability, seam cell development, and vulval development in Caenorh

32 hroughout C. elegans development to regulate seam cell differentiation and cell fusion.

33 that puf-9 and let-7 may mediate hypodermal seam cell differentiation by regulating common targets.

34 hat regulates a late-stage aspect of uterine seam cell differentiation that specifically affects anch

35 described herein cause delays in vulval and seam cell differentiation, indicating a role for lin-66

36 last larval stage (L4), following the final seam cell division, which occurs during the L3-to-L4 mol

37 n-23 mutants the phenotypes of supernumerary seam cell divisions, defective alae formation, and the a

38 al differentiation of the lateral hypodermal seam cells during the larval-to-adult molt.

39 vitro, and this site is necessary for robust seam cell expression in vivo.

40 am cell specification, and for hypodermal to seam cell fate transformations induced by ectopic Wnt pa

41 on causes the precocious expression of adult seam cell fates.

42 abnormalities in vulval lineage and uterine seam-cell formation.

43 hat specifically affects anchor cell-uterine seam cell fusion.

44 s, a row of epidermal precursor cells called seam cells generates a pattern of cuticular alae in ante

45 of driving extra cell divisions, leading to seam cell hyperplasia.

46 were expressed exclusively in the intestine, seam cells, hypodermal cells of the main body syncytium,

47 Seam cells in affected animals do not differentiate prop

48 Seam cells in affected animals often undergo inappropria

49 nts, all epidermal cells, except the lateral seam cells, inappropriately fuse into a single large syn

50 find that OSM-11 is secreted from hypodermal seam cells into the pseudocoelomic body cavity and acts

51 Ectopic expression of LECT-2 from seam cells is sufficient to redirect the PVD dendrites o

52 specificity of cell fates in the hypodermal seam cell lineages.

53 f-renewing and proliferative behavior in the seam cell lineages.

54 , we used the postembryonic epithelial stem (seam) cell lineages of Caenorhabditis elegans.

55 remains unchanged when nmy-2 is inactivated, seam cell loss occurs through inappropriate terminal dif

56 al 23 deficiencies blocked expression of the seam cell marker, in some cases without preventing cell

57 Here, we report that a gene required for seam cell maturation is also required for specification

58 ng polarised growth of vulval precursors and seam cells, migrations of neuroblasts and axons, and the

59 e earliest detectable LIN-29 accumulation in seam cell nuclei is during the last larval stage (L4), f

60 uring development, which affect the terminal seam cell number in opposing directions.

61 -helix (bHLH) transcription factor, increase seam cell number variability.

62 ermis, is often ectopically expressed in the seam cells of affected animals, demonstrating that ELT-5

63 pparatus occurring exclusively in hypodermal seam cells, pharyngeal cells, and spermatheca.

64 e main hypodermal syncytium, indicating that seam cells play the major role in secreting surface coat

65 ress pal-1 and in the neighboring hypodermal seam cell precursors, which do not, as well as in poster

66 seven deficiencies had no apparent effect on seam cell production, 21 were found to result in subnorm

67 d that rnt-1 is a rate-limiting regulator of seam cell proliferation in C. elegans, as overexpression

68 e is that all are expressed most strongly in seam cells, rather than in the main hypodermal syncytium

69 that two GATA factors that are required for seam cell specification in the embryo independently of W

70 iously been shown to be required for initial seam cell specification in the embryo.

71 egl-18 and elt-6 are necessary for larval seam cell specification, and for hypodermal to seam cell

72 lin-4, the lin-58 mutations cause precocious seam cell terminal differentiation and thus define a new

73 The let-7 miRNA times seam cell terminal differentiation in C. elegans.

74 -29 specify the timing of lateral hypodermal seam cell terminal differentiation in Caenorhabditis ele

75 mutations also restore other aspects of the seam cell terminal differentiation program that are defe

76 because of mutation of lin-4, which prevents seam cell terminal differentiation.

77 NCX-9 functions in hypodermal seam cells that secrete the axon guidance cue UNC-129/BM

78 ne controls gene expression in the epidermal seam cells, uterus and vulva, and may help to coordinate

79 ns uterine anchor cell (AC) with the uterine-seam cell (utse) is an excellent model system for studyi

80 The Caenorhabditis elegans uterine seam cell (utse) is an H-shaped syncytium that connects

81 egans, six lateral epidermal stem cells, the seam cells V1-V6, are located in a row along the anterio

82 Anterior seam cells (V1-V4) undergo a fairly simple sequence of s

83 Posterior seam cells (V5 and V6) undergo a more complicated sequen

84 Hox gene mab-5 is required for two posterior seam cells, V5 and V6, to generate rays.

85 d during the last larval stage in hypodermal seam cells which is transcriptionally regulated by hbl-1

86 hormone receptor daf-12 is a let-7 target in seam cells, while the forkhead transcription factor pha-

87 g larval development can cause fusion of all seam cells with the surrounding syncytia and pronounced

88 vestigate the translational potential of the SEAM, cells within it that resemble ocular-surface epith