Ward J G, Davis M C, Allis C D, Herrick G
University of Utah School of Medicine, Salt Lake City 84132, USA.
Genetics. 1995 Jul;140(3):989-1005. doi: 10.1093/genetics/140.3.989.
Conjugation fails postzygotically after mating of Tetrahymena cells that have wild-type parental macronuclei but harbor noncomplementing nullisomic parental germline deficiencies. Failures begin shortly after formation of the new macronuclear precursor (anlage) and completion of the first step in elimination of the parental macronucleus (pycnosis). Conjugants fail to complete pair separation, to eliminate one new micronucleus, and to amplify anlage DNA, and they eventually die. Some deficiencies block resorption of the pycnotic parental macronucleus, but we find no evidence for its regeneration. Some deficiencies cause aberrant anlage DNA loss. Those that do not cause DNA loss are epistatic to those that do, indicating that normal anlage development requires the dependent function of at least two types of genes. The possibility that these genes are involved in developmentally regulated anlage DNA rearrangements is discussed. Each observed conjugation defect indicates insufficiency of the parental macronucleus to direct postzygotic development and can be explained by the deficiency of essential conjugation genes that are expressed from the anlage. The failure of nullisomic conjugants to complete pair separation indicates a requirement for gene products, expressed from the early anlage or its precursors, soon after anlage first differentiate.
在具有野生型亲代大核但携带非互补零体亲代种系缺陷的四膜虫细胞交配后，接合在合子后失败。失败在新的大核前体（原基）形成以及亲代大核消除的第一步（固缩）完成后不久就开始了。接合体无法完成配对分离、消除一个新的微核以及扩增原基DNA，最终死亡。一些缺陷会阻止固缩的亲代大核的吸收，但我们没有发现其再生的证据。一些缺陷会导致异常的原基DNA丢失。不导致DNA丢失的缺陷对导致DNA丢失的缺陷具有上位性，这表明正常的原基发育需要至少两种类型基因的依赖性功能。讨论了这些基因参与发育调控的原基DNA重排的可能性。每个观察到的接合缺陷都表明亲代大核不足以指导合子后发育，并且可以通过从原基表达的必需接合基因的缺陷来解释。零体接合体无法完成配对分离表明在原基首次分化后不久就需要从早期原基或其前体表达的基因产物。
