ライフサイエンスコーパス: gonocyte

1 w that MIWI2 associates with TEX15 in foetal gonocytes.

2 hat enter meiosis synchronously with ovarian gonocytes.

3 on of cells that express markers specific to gonocytes.

4 associates with SPOCD1 and C19ORF84 in fetal gonocytes.

5 nd found that Foxo1 specifically marks mouse gonocytes and a subset of spermatogonia with stem cell p

6 ombination are born with significantly fewer gonocytes and exhibit defective spermatogenesis and redu

7 o ablate Sin3a from perinatal quiescent male gonocytes and from postnatal differentiating spermatogon

8 t UTF1 is expressed in embryonic and newborn gonocytes and in a subset of early spermatogonia.

9 s being born with severely reduced number of gonocytes and oocytes.

10 ling the proliferation or differentiation of gonocytes and spermatogonia and possibly the somatic lin

11 Zfp145 expression was restricted to gonocytes and undifferentiated spermatogonia and was abs

12 ized that maintenance and differentiation of gonocytes and/or spermatogonial stem cells would be modu

13 cellular microenvironment, were followed by gonocyte apoptosis and near complete disappearance of th

14 In mice, the SSC pool arises from gonocytes approximately 6 days after birth.

15 Gonocytes are a transient population of male germ-line s

16 mulatively, our findings indicate that early gonocytes are in a dual poised, bipotential state in whi

17 beginning at approximately 2 months of age, gonocytes are replaced by adult dark (Ad) and pale (Ap)

18 m neonatal transgenic rats demonstrated that gonocytes are the only cells that express a lacZ reporte

19 e by in situ hybridization in fetal day 15.5 gonocytes but was detectable at a low abundance by RT-PC

20 Sin3a is required for the mitotic reentry of gonocytes, but is dispensable for the maintenance of dif

21 tosis and near complete disappearance of the gonocytes by day 2 after birth.

22 In contrast to spermatogonial stem cells, gonocytes can be identified easily in neonatal rat testi

23 evated in both human spermatogonia and mouse gonocytes compared to somatic cells.

24 Our results demonstrate that gonocytes differently from mature spermatogonia exhibit

25 In addition, conditional ablation of NRF1 in gonocytes dramatically down-regulated these germline gen

26 provide new information on the regulation of gonocyte fate and exciting new evidence supporting a lin

27 on around E6.25, fetal piRNAs emerge in male gonocytes from E13.5 onward.

28 We observed aberrant exit of gonocytes from mitotic arrest, migration toward cord per

29 Since surviving gonocytes give rise to subsequent generations of germ ce

30 of neonatal testes containing Sin3a-deleted gonocytes identified upregulated transcripts highly asso

31 oli cells is required for the maintenance of gonocytes in an undifferentiated state during fetal deve

32 B-cadherin (STPB-C) in promoting survival of gonocytes in neonatal rats and we have linked its expres

33 led delayed and defective differentiation of gonocytes into SSCs.

34 ber of critical events including re-entry of gonocytes into the cell cycle and eventual loss of many

35 The metabolism of gonocytes is not defined.

36 of early prepubertal porcine spermatogonia (gonocytes) is characterized by the reliance on OXPHOS fu

37 In contrast, perinatal gonocytes lacking Sin3a underwent rapid depletion that c

38 differentiated), induction of multinucleated gonocytes (MNGs), and aggregation of differentiated germ

39 functional changes that drastically affected gonocyte numbers and physiology.

40 The B-myb mRNA is expressed most highly in gonocytes of the fetal testis and in spermatogonia and e

41 Together, the pseudopod and round gonocyte populations will provide powerful tools for the

42 rogramming and differentiate into oogonia or gonocytes, precursors for oocytes or spermatogonia, resp

43 e spermatogonial stem cell (SSC) precursors (gonocytes) present in the testis for an extended period

44 f a spermatogonial stem cell (SSC) pool from gonocyte progenitors, and thereafter balancing SSC renew

45 gically normal; however, at post-natal day 3 gonocyte proliferation is impaired and expression of spe

46 genetic ablation of Brg1 in murine embryonic gonocytes results in arrest during prophase of meiosis I

47 ation of germ cell apoptosis and survival in gonocyte-Sertoli cell co-cultures, and direct study of t

48 present almost exclusively in the pseudopod gonocyte subpopulation.

49 Two gonocyte subpopulations, designated pseudopod and round,

50 11.5 dpc, and that FGF9 directly promotes XY gonocyte survival after 11.5 dpc, independently from Ser

51 FGF9 is necessary for 11.5 dpc XY gonocyte survival and is the earliest reported factor wi

52 th prepubertal human spermatogonia and mouse gonocytes than in somatic cells.

53 ale germ cell development is crucial for the gonocyte-to-spermatogonia transition and long-term sperm

54 and adult testes, p53R172H was expressed in gonocytes, type A, Int, B spermatogonia as well as in pr

55 n germ cells with increasing expression from gonocytes/type A spermatogonia to pachytene spermatocyte

56 taining indicated that the majority of round gonocytes undergo apoptosis.

57 fine the interactome of MIWI2 in mouse fetal gonocytes undergoing de novo genome methylation and iden

58 of prepubertal human spermatogonia and mouse gonocytes were selected from testis biopsies and validat

59 LCs do not yet resemble E13.5 or later mouse gonocytes where the piRNA pathway is active.