Kaczanowski A, Kaczanowska J
Department of Cytophysiology, University of Warsaw, Poland.
J Eukaryot Microbiol. 1996 Sep-Oct;43(5):380-8. doi: 10.1111/j.1550-7408.1996.tb05047.x.
During conjugation, the micronucleus of Tetrahymena thermophila undergoes five consecutive nuclear divisions: meiosis, third prezygotic division (pregamic mitosis) and two postzygotic mitoses of the synkaryon. The four products of the synkaryon differentiate into macronuclear anlagen and new micronuclei and the old macronucleus is resorbed. The protein synthesis inhibitor cycloheximide, applied during conjugation, induced several developmental blocks. Pairs shifted to the drug during early meiotic prophase (stages I-III) were arrested at prophase. Cycloheximide applied to cells at pachytene (stages IV-VI) to metaphase arrested the conjugants at the stage of modified prometaphase/metaphase with overcondensed, swollen bivalents. In contrast to other systems, in the presence of cycloheximide, separation of chromatids, decondensation of chromosomes and exit from metaphase I were inhibited in both diploid and haploid cells. Pairs shifted to the drug after metaphase I were arrested at postmeiotic interphase after completing one nuclear cycle. The same rule applied to the subsequent cycle; then cells were arrested at the stage of pronuclei, and those pairs with functional pronuclei and synkarya were arrested at the stage of two products of the first postzygotic division (pronuclei were not arrested in nuclear transfer and karyogamy). Only pairs with two products of the first postzygotic division were arrested at the same stage after the cycloheximide treatment. Pairs shifted to cycloheximide during the second postzygotic division were arrested in development of macronuclear anlagen and resorption of old macronuclei. The postmeiotic conjugants pulse-treated with cycloheximide (2 h) yielded heterokaryons retaining parental macronuclei (i.e. they exhibited macronuclear retention).
在接合过程中，嗜热四膜虫的微核经历连续五次核分裂：减数分裂、第三次合子前分裂（合子前有丝分裂）以及合核体的两次合子后有丝分裂。合核体的四个产物分化为大核原基和新的微核，而旧的大核则被吸收。在接合过程中应用蛋白质合成抑制剂环己酰亚胺会导致几个发育阻滞。在减数分裂前期早期（I - III期）转移到该药物的细胞对停滞在前期。在粗线期（IV - VI期）到中期应用环己酰亚胺会使接合体停滞在修饰的前中期/中期阶段，此时二价体过度浓缩、肿胀。与其他系统不同的是，在环己酰亚胺存在的情况下，二倍体和单倍体细胞中染色单体的分离、染色体的解聚以及从中期I退出均受到抑制。在中期I后转移到该药物的细胞对在完成一个核周期后停滞在减数分裂后间期。同样的规则适用于随后的周期；然后细胞停滞在原核阶段，而那些具有功能性原核和合核体的细胞对则停滞在第一次合子后分裂的两个产物阶段（在核转移和核融合中原核不会停滞）。只有具有第一次合子后分裂的两个产物的细胞对在环己酰亚胺处理后停滞在同一阶段。在第二次合子后分裂期间转移到环己酰亚胺的细胞对在大核原基的发育和旧大核的吸收过程中停滞。用环己酰亚胺脉冲处理（2小时）的减数分裂后接合体产生保留亲本大核的异核体（即它们表现出大核保留）。
