Effects of the transcription inhibitor actinomycin D on postzygotic development of Tetrahymena thermophila conjugants

• Published in: Developmental biology 1996-01, Vol.173 (1), p.174-184
• Main Authors: Ward, J G, Herrick, G
• Format: Article
• Language: English
• Subjects: Animals; Cell Nucleus - drug effects; Cell Nucleus - physiology; Conjugation, Genetic; Cycloheximide - pharmacology; Dactinomycin - pharmacology; DNA, Protozoan - metabolism; Gene Expression; Protein Synthesis Inhibitors - pharmacology; Tetrahymena; Tetrahymena thermophila - drug effects; Tetrahymena thermophila - growth & development; Tetrahymena thermophila - ultrastructure; Time Factors; Transcription, Genetic - drug effects; Zygote - drug effects; Zygote - growth & development; Zygote - ultrastructure
• ISSN: 0012-1606
• DOI: 10.1006/dbio.1996.0015

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.