Sluder G, Miller F J, Lewis K
Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545.
Dev Biol. 1993 Jan;155(1):58-67. doi: 10.1006/dbio.1993.1006.
Although both gametes may contribute a centrosome to the zygote at fertilization, only one of these centrosomes is used in development. Thus, specific mechanisms must exist to control centrosome inheritance in all sexually reproducing organisms. We use starfish as a model system to characterize these control mechanisms because the eggs complete meiosis I and meiosis II after fertilization; this allows us to directly follow the fate of all parental centrosomes in vivo. Only the paternal centrosome is used in starfish development. Although the microtubule organizing center activity of the maternal centrosome persists, the functional loss of this centrosome involves the suppression of its ability to double, or reproduce, at successive mitoses (Sluder et al., 1989. Dev. Biol. 131, 567-579). To determine when the reproductive capacity of the maternal centrosome is degraded, we transfer meiosis I and meiosis II spindles from just fertilized eggs into other zygotes that are in prophase of first mitosis. Meiosis I spindles are stable during first mitosis and are disassembled in first telophase in concert with the host spindle. In 61% of the cases a variable number of formerly meiotic centrosomes are active at second mitosis and reproduce in a normal fashion between subsequent mitoses. However, when meiosis II spindles are transferred in the same manner, in only 26% of the cases do any of the centrosomes persist past first mitosis or reproduce in a normal fashion thereafter. In the remainder of the cases the remnants of the maternal centrosomes organize a single monaster that does not double between mitoses. Control transfers of first mitosis spindles indicate that these results are not due to nonspecific damage to the meiotic spindles or to the recipient zygotes. These observations indicate that the reproductive capacity of maternal centrosomes is degraded during meiosis I, not during oogenesis. Our results also show that the cytoplasmic conditions which eliminate this reproductive capacity are no longer active once the zygote has entered the first mitotic cell cycle.
尽管在受精时两个配子可能都会为受精卵贡献一个中心体，但在发育过程中只有其中一个中心体被使用。因此，在所有有性生殖的生物体中必然存在特定的机制来控制中心体的遗传。我们以海星作为模型系统来表征这些控制机制，因为海星的卵子在受精后完成减数分裂I和减数分裂II；这使我们能够在体内直接追踪所有亲代中心体的命运。在海星发育过程中只有父本中心体被使用。尽管母本中心体的微管组织中心活性持续存在，但该中心体的功能丧失涉及到其在连续有丝分裂时加倍或复制能力的抑制（斯卢德等人，1989年。《发育生物学》131卷，567 - 579页）。为了确定母本中心体的复制能力何时退化，我们将刚受精卵子的减数分裂I和减数分裂II纺锤体转移到处于第一次有丝分裂前期的其他受精卵中。减数分裂I纺锤体在第一次有丝分裂期间是稳定的，并在第一次末期与宿主纺锤体一起解体。在61%的情况下，数量不等的先前减数分裂的中心体在第二次有丝分裂时是活跃的，并在随后的有丝分裂之间以正常方式复制。然而，当以同样的方式转移减数分裂II纺锤体时，只有26%的情况下任何中心体能够在第一次有丝分裂后持续存在或以正常方式复制。在其余的情况下，母本中心体的残余物组织形成一个单星体，在有丝分裂之间不会加倍。第一次有丝分裂纺锤体的对照转移表明，这些结果不是由于减数分裂纺锤体或受体受精卵受到非特异性损伤所致。这些观察结果表明，母本中心体的复制能力在减数分裂I期间退化，而不是在卵子发生期间。我们的结果还表明，一旦受精卵进入第一个有丝分裂细胞周期，消除这种复制能力的细胞质条件就不再起作用。
