Effects of the transcription inhibitor actinomycin D on postzygotic development of Tetrahymena thermophila conjugants
Effects of the transcription inhibitor actinomycin D on postzygotic development of Tetrahymena thermophila conjugants
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DOI：
10.1006/dbio.1996.0015
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发表时间：
1996-01-10
影响因子：
2.7
通讯作者：
Herrick, G
中科院分区：
文献类型：
--
作者：
Ward, JG;Herrick, G
在嗜热四膜虫接合过程中，新的体细胞大核从一个共同的合子核发育而来，而旧的亲本体细胞核被破坏。转录抑制剂放线菌素D破坏许多合子后接合的事件（放线菌酮引起不可区分的影响）。早期治疗导致所有合子后发育的阻断，表明接合子通过检查点的转录要求，允许进入合子后发育。此后，如果在这些事件正常发生前至少1.5小时加入放线菌素D，则可阻断配对分离、旧大核的吸收和新微核之一的消除。在发育中的大核（原基）中DNA重排之前的处理导致异常原基DNA丢失，这表明这种DNA丢失可能是由基因组重排中涉及的基因表达的抑制引起的。DNA丢失和相关的致死性似乎需要先前的基因表达，因为较早加入的放线菌素D导致细胞在发育中停滞而无原基DNA丢失，并且一旦放线菌素D被去除，这些接合物可以（以一定频率）完成接合并产生可存活的后代。旧的大核已经被灭活之前，大多数放线菌素D治疗开始，表明我们观察到的各种诱导的缺陷是抑制合子后基因表达的结果，大概在原基。由放线菌素D诱导的缺陷类似于先前在含有缺体生殖系缺陷但成熟的老大核的接合子中观察到的缺陷。(C)出版社：Academic Press，Inc.
During Tetrahymena thermophila conjugation, new somatic macronuclei develop from a common zygotic nucleus derived from meiotic products of the germline, and the old parental somatic nucleus is destroyed. The transcription inhibitor actinomycin D disrupts many events of postzygotic conjugation (cycloheximide causes indistinguishable effects). Early treatment causes a block of all postzygotic development, suggesting a transcription requirement for conjugants to pass a checkpoint, allowing entry into postzygotic development. Thereafter, pair separation, resorption of the old macronucleus, and elimination of one of the new micronuclei are blocked if actinomycin D is added at least 1.5 hr before each of these events normally occurs. Treatment just before DNA rearrangements in the developing macronuclei (anlagen) causes aberrant anlage DNA loss, suggesting that this DNA loss may be caused by inhibition of gene expression involved in genome rearrangements. DNA loss, and correlated lethality, appear to require previous gene expression, since actinomycin D added earlier causes cells to arrest in development without anlage DNA loss, and these conjugants can (at some frequency) complete conjugation and make viable progeny once actinomycin D is removed. The old macronucleus already had been inactivated before most actinomycin D treatments were initiated, indicating that the various induced defects we observed are the result of inhibition of postzygotic gene expression, presumably in anlagen. The defects induced by actinomycin D are similar to defects previously observed in conjugants harboring nullisomic germline deficiencies but proficient old macronuclei. (C) 1996 Academic Press, Inc.