Liu Lin, Blasco Maria A, Keefe David L
Department of Obstetrics and Gynecology, Women and Infants Hospital, Brown University, Providence, RI 02905, USA.
EMBO Rep. 2002 Mar;3(3):230-4. doi: 10.1093/embo-reports/kvf055.
Telomerase deficiency in the mouse eventually leads to loss of telomeric repeats from chromosome ends and to end-to-end chromosome fusions, which result in defects in highly proliferative tissues. We show that telomere dysfunction resulting from telomerase deficiency leads to disruption of functional meiotic spindles and misalignment of chromosomes during meiotic division of oocytes in late-generation (G4) mice. However, oocytes from first-generation (G1) mice lacking telomerase showed no appreciable telomere dysfunction and exhibited chromosome alignment at the metaphase plates of meiotic spindles, in a manner similar to that of wild-type mouse oocytes. These findings suggest that telomerase does not directly influence chromosome alignment and spindle integrity. Rather, functional telomeres may be involved in mediating metaphase chromosome alignment and maintaining functional spindles during meiotic division.
小鼠中的端粒酶缺陷最终会导致染色体末端的端粒重复序列丢失,并导致染色体端端融合,这会在高度增殖的组织中产生缺陷。我们发现,端粒酶缺陷导致的端粒功能障碍会导致晚期(G4)小鼠卵母细胞减数分裂期间功能性减数分裂纺锤体的破坏和染色体错排。然而,缺乏端粒酶的第一代(G1)小鼠的卵母细胞没有明显的端粒功能障碍,并且在减数分裂纺锤体的中期板上呈现染色体排列,其方式与野生型小鼠卵母细胞相似。这些发现表明,端粒酶不会直接影响染色体排列和纺锤体完整性。相反,功能性端粒可能参与介导减数分裂中期染色体排列,并在减数分裂期间维持功能性纺锤体。