ライフサイエンスコーパス: epaxial

1 nocytes are differentially restricted to the epaxial and hypaxial body domains, respectively.

2 owth in the myotome specifically, and in the epaxial and hypaxial domains of the body generally, are

3 Myotome formation in the epaxial and hypaxial domains of thoraco-lumbar somites w

4 and maintain the medio-lateral boundaries of epaxial and hypaxial gene expression.

5 tial role in maintaining the balance between epaxial and hypaxial muscle mass.

6 Epaxial and hypaxial muscle precursors can be attributed

7 quently inhibiting all further growth of the epaxial and hypaxial myotome.

8 Muscle precursor cells for the epaxial and hypaxial myotomes are predominantly located

9 ard and ventralward growth directions of the epaxial and hypaxial myotomes.

10 relies on segregated, separately innervated epaxial and hypaxial skeletal muscles.

11 rete enhancers that drive Myf5 expression in epaxial and hypaxial somites, branchial arches and centr

12 onates, dramatic losses were observed in the epaxial and hypaxial trunk muscles that are proximal to

13 Shh-/- embryos is suppressed not only in the epaxial but also in the hypaxial myotomes, while it is m

14 ion of Myf5, leading to the determination of epaxial dermomyotomal cells to myogenesis, as well as tr

15 MyoD, is the target of Shh signaling in the epaxial dermomyotome, as MyoD activation by recombinant

16 myogenic specification and for growth of the epaxial domain during early embryonic development.

17 nesis of the myotome and dermomyotome in the epaxial domain of the body.

18 es the first phase of Myf5 expression in the epaxial domain of the somite, in order to identify the s

19 scle to organize, the primary myotome of the epaxial domain, is a thin sheet of muscle tissue that ex

20 Myf5 epaxial expression, driven by the early epaxial enhancer in the dermomyotome, is necessary for e

21 rapidly from those that impinge on the early epaxial enhancer to those that impinge on the other enha

22 ntrol of an element we have called the early epaxial enhancer.

23 We propose that the first phase of Myf5 epaxial expression, driven by the early epaxial enhancer

24 , the En1-Sim1 expression boundary marks the epaxial-hypaxial dermomyotomal or myotomal boundary.

25 division and hence the formation of distinct epaxial-hypaxial muscles is not understood.

26 true compartment boundary, foreshadowing the epaxial-hypaxial segregation of muscle.

27 y continuous dermomyotome and myotome, whose epaxial-hypaxial subdivision and hence the formation of

28 al compartments, which correspond to neither epaxial/hypaxial nor primaxial/abaxial subdivisions.

29 The epaxial/hypaxial terminology is also used to describe re

30 ral patterning for Gli family members in the epaxial induction of Myf5 expression.

31 om the nerve, whereas we recently found that epaxial melanocytes segregate earlier from Foxd3-positiv

32 dermomyotome give rise to dorsal dermis and epaxial muscle and, unexpectedly, to interscapular brown

33 ls restrict hypaxial development and promote epaxial muscle formation.

34 Dorsal dermis and epaxial muscle have been shown to arise from the central

35 The apoptosis of epaxial muscle in somites that formed after notochord de

36 rate enhancers controlling expression in the epaxial muscle precursors of the body, some hypaxial pre

37 li3 in the control of Myf5 activation in the epaxial muscle progenitor cells and in dorsoventral and

38 hancer, is required for the specification of epaxial muscle progenitor cells.

39 Gli3 is required for Myf5 activation in the epaxial muscle progenitor cells.

40 activation of Myf5 expression in the somite epaxial muscle progenitors in mouse embryos.

41 ssion in the specification of dorsal somite, epaxial muscle progenitors.

42 l compartments, which contain progenitors of epaxial muscle, dermis and hypaxial muscle, respectively

43 uced in myotomally derived muscles including epaxial muscles (deep back muscles) and hypaxial muscles

44 ate the CNS network that controls the lumbar epaxial muscles that produce this posture.

45 After PRV was injected into lumbar epaxial muscles, the time course analysis of CNS viral i

46 ed with significantly decreased formation of epaxial muscles.

47 tion, and that this response is the same for epaxial myoblasts.

48 ts suggest that Wnt/Lef1 signaling regulates epaxial myogenesis via Pitx2 but that this link is uncou

49 support of the inductive function of Shh in epaxial myogenesis, we show that Shh is not essential fo

50 In mice, Myf5 is essential for the earliest epaxial myogenesis, whereas Myod is required for timely

51 transcripts are expressed in Myf5-expressing epaxial myogenic progenitors in the dorsal medial dermom

52 ial for the survival or the proliferation of epaxial myogenic progenitors.

53 The precursors to the embryonic epaxial myotome are concentrated in the dorsomedial lip

54 Therefore, models of epaxial myotome formation must account for the positioni

55 antly, Myf5 is subsequently expressed in the epaxial myotome under the control of other elements loca

56 ckground, myoblasts derived from the medial (epaxial) myotome are not present to compensate for defic

57 on in the expression of Myf5 and MyoD in the epaxial myotomes, but not in the hypaxial myotomes.

58 Its structures are categorized as epaxial or hypaxial based on their adult position and in

59 or the early growth and morphogenesis of the epaxial primary myotome and the overlying dermomyotome e

60 increases myocyte number particularly in the epaxial region of the myotome.

61 This dependence on epaxial signals and suppression by hypaxial signals plac

62 n were present in unaffected neural tube and epaxial somatic component.

63 th Gli2 and Zic1 in transactivating the Myf5 epaxial somite (ES) enhancer in concert with the Myf5 pr

64 This Myf5 epaxial somite (ES) enhancer is Shh-dependent, as shown

65 ia an essential Gli-binding site in the Myf5 epaxial somite (ES) enhancer, is required for the specif

66 regulated by canonical Wnt signaling in the epaxial somite and second branchial arch, but not in the

67 ent is necessary for expression in the early epaxial somite but in no other site of myogenesis.

68 c determination genes, Myf5 and MyoD, in the epaxial somite cells that give rise to the progenitors o

69 reporter gene under the control of the Myf5 epaxial somite enhancer, we show that Gli2 or Gli3 is re

70 Zic genes have a role in Myf5 regulation for epaxial somite myogenesis in the mouse embryo.

71 hh signaling in transfected 3T3 cells and in epaxial somite progenitors in transgenic embryos.

72 on the other enhancers that act later in the epaxial somite, indicating that there are significant ch

73 te the transactivation of Gli-dependent Myf5 epaxial somite-specific (ES) enhancer activity in 3T3 ce

74 h Zic1 and Gli2 to transactivate Myf5 in the epaxial somite.

75 tors are required for Myf5 expression in the epaxial somite.

76 sion by hypaxial signals places En1 into the epaxial somitic programme.

77 ws that myotome growth begins earlier in the epaxial than in the hypaxial domain, but that after an i

78 rmomyotome and a shift in myoblast fate from epaxial to hypaxial, eventually leading to an excess of