ライフサイエンスコーパス: polar cell

1 ctivated form of Notch can generate an extra polar cell.

2 ar epithelium with a peak at its source, the polar cells.

3 osis in existing polar cells to induce extra polar cells.

4 switch in Fasciclin 2 polarity in the inner polar cells.

5 ause epithelial follicle cells to develop as polar cells.

6 e is re-oriented with respect to the ectopic polar cells.

7 in follicle formation appears to map to the polar cells.

8 ects in the specification of stalk cells and polar cells.

9 ization, but not specification, of stalk and polar cells.

10 Here we report that the polar cells--a group of follicle cells differentiated ea

11 Our observations demonstrate that the polar cells act as an organizer that patterns surroundin

12 This lineage goes on to make two cell types: polar cells and stalk cells.

13 Clones of cells mutant for Notch also lack polar cells and the requirement for Notch in follicle fo

14 ment for fringe in follicle formation to the polar cells, and demonstrates that fringe is required fo

15 ore propose a model in which stalk cells and polar cells are derived from a precursor population that

16 Moreover, when polar cells are mislocalized laterally, the surrounding

17 , during budding, stalk cells and additional polar cells are specified in a process that frequently t

18 Both anterior and posterior polar cells arise in region 2b at a time when approximat

19 We found that the Notch-induced extra polar cells arise through recruitment of the neighboring

20 cell becomes the R3 photoreceptor while the polar cell becomes the R4 photoreceptor.

21 d the anterior-posterior axis defined by the polar cells, but mutations in Lar frequently disrupt pol

22 Conversely, increasing the number of polar cells by expressing an activated form of the Notch

23 athway, which triggers the relaxation of the polar cell cortex at mid anaphase.

24 fy genes that affect the localization of two polar cell cycle histidine kinases, PleC and DivJ, and t

25 DivJ, a regulator of polar cell development, is necessary for maintaining low

26 lls, but mutations in Lar frequently disrupt polar cell differentiation and actin polarization.

27 hat contributes to the switch from medial to polar cell division during sporulation and is responsibl

28 is a membrane protein that localizes to the polar cell division sites where it causes FtsZ to reloca

29 y events of spore development, including the polar cell division, with successful completion of chrom

30 s be traced back to the specification of the polar cells during early oogenesis.

31 ylation is not as severe but also results in polar cell elongation and differentiation defects.

32 pe I activity is required for cell adhesion, polar cell elongation, and cell differentiation.

33 and culminates in the biosynthesis of a thin polar cell envelope extension called the stalk.

34 but interrelated developmental pathways for polar cell envelope synthesis and positional information

35 n family, ADL1A and ADL1E, are essential for polar cell expansion and cell plate biogenesis.

36 y load onto microtubule plus ends and direct polar cell expansion and organ growth in response to dir

37 Polar cell expansion in differentiating tissues is criti

38 t the tip growth mechanism also may modulate polar cell expansion in differentiating tissues.

39 Root hairs develop by polar cell expansion or tip growth, a unique mode of pla

40 like fungal hyphae, possess a typical tip or polar cell expansion with growth limited to the apical d

41 alleles (scd1-2 and scd1-3) markedly affect polar cell expansion, most notably in trichomes and root

42 negative mutant for ROP2 (DN-rop2) inhibited polar cell expansion, whereas the expression of a consti

43 its roles in cell polarity establishment and polar cell expansion.

44 ted vesicle transportation is sufficient for polar cell extension, but in S. pombe, MTs are in additi

45 sion of EYA is capable of suppressing normal polar cell fate and compromising the normal functions of

46 nor the decision between the stalk cell and polar cell fate but, rather, some later differentiation

47 and Gro promote differentiation towards the polar cell fate by promoting Notch pathway activity.

48 e eyes absent (eya) to be a key repressor of polar cell fate.

49 and demonstrates that fringe is required for polar cell fate.

50 g signaling, which is known to cause ectopic polar cell formation, does so by repressing eya expressi

51 cterization of mutants that affect stalk and polar cell formation.

52 account for the defects in cell adhesion and polar cell growth control observed in the mutants.

53 Polar cell growth is sustained by oscillatory feedback l

54 ion of actin and other proteins required for polar cell growth of filaments but not for the basic str

55 Pollen tube elongation is a polar cell growth process dependent on an active and tig

56 Adhesion between motile cells and polar cells holds the cluster together and polarizes eac

57 udy of pHLIP-mediated cellular delivery of a polar cell-impermeable toxin, alpha-amanitin, an inhibit

58 ants revealed a failure in the fusion of the polar cells in embryo sac development, in addition to em

59 oogenesis, and establish a function for the polar cells in separating germline cysts into individual

60 in the FE, uniformly expressed except in the polar cells, is established by Notch signaling around st

61 e together with meropenem resulted in rapid, polar, cell lysis releasing cytoplasmic contents.

62 We propose that Upd secreted from the polar cells may act as a morphogen to stimulate A/P-deri

63 The polar cells occupy the termini of the follicle and are s

64 lost in outer border cells, but not in inner polar cells of the cluster.

65 ct of these chambers is the expansion of the polar cell population and concomitant loss of interfolli

66 ht green fluorescent, presumably actin-rich, polar cell proboscis that inserts itself into the formin

67 Normally, differentiation of the polar cells requires Notch signaling.

68 At the posterior, elimination of polar cells results in abnormal oocyte localization.

69 This genetic ablation of polar cells results in cell fate defects within surround

70 anterior polar follicle cells, the anterior polar cells signal through the JAK/STAT pathway to induc

71 marium intercyst cells that are required for polar cell specification and differentiation.

72 least three types of somatic follicle cells, polar cells, stalk cells and main body epithelial follic

73 lls (FSCs) in each ovariole give rise to all polar cells, stalk cells, and main body cells needed to

74 ate and compromising the normal functions of polar cells, such as promotion of border cell migration.

75 his may account for the formation of ectopic polar cells, the extended proliferation of follicle cell

76 obably involved in down-regulating String in polar cells, thus inducing the G2 cell-cycle arrest.

77 on of String can trigger mitosis in existing polar cells to induce extra polar cells.

78 sions of polarised blastomeres that allocate polar cells to outer and apolar cells to inner positions

79 ion at sites where it accumulates due to its polar, cell-to-cell transport [2-6].

80 Plant architecture is influenced by the polar, cell-to-cell transport of auxin that is primarily

81 n-optimized thioesterase genes and weakening polar cell wall layers.

82 hatase Cdc25 homolog, and Notch signaling in polar cells, we found that misexpression of String can t

83 Small, restricted clones in stalk cells and polar cells were found adjacent to each other at a frequ