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A pronounced R22-induced formation of nuclear speckled aggregation of pUL69 was demonstrated. Multi-labelling confocal laser-scanning microscopy revealed that CDK9 and cyclin T1 co-localized perfectly with pUL69 in individual speckles. The effects were similar to those described recently for the broad CDK inhibitor roscovitine. Co-immunoprecipitation and yeast two-hybrid analyses showed that cyclin T1 interacted with both CDK9 and pUL69. The interaction region of pUL69 for cyclin T1 could be attributed to aa 269\u2013487. Moreover, another component of CDK inhibitor-induced speckled aggregates was identified with RNA polymerase II, supporting earlier reports that strongly suggested an association of pUL69 with transcription complexes. Interestingly, when using a UL69-deleted recombinant HCMV, no speckled aggregates were formed by CDK inhibitor treatment. This indicated that pUL69 is the defining component of aggregates and generally may represent a crucial viral interactor of cyclin T1. In conclusion, these data emphasize that HCMV inter-regulation with CDK9\/cyclin T1 is at least partly based on a pUL69\u2013cylin T1 interaction, thus contributing to the importance of CDK9 for HCMV replication.<\/jats:p>","DOI":"10.1099\/vir.0.030494-0","type":"journal-article","created":{"date-parts":[[2011,3,31]],"date-time":"2011-03-31T02:29:52Z","timestamp":1301538592000},"page":"1519-1531","source":"Crossref","is-referenced-by-count":33,"title":["Recruitment of cyclin-dependent kinase 9 to nuclear compartments during cytomegalovirus late replication: importance of an interaction between viral pUL69 and cyclin T1"],"prefix":"10.1099","volume":"92","author":[{"given":"Sabine","family":"Feichtinger","sequence":"first","affiliation":[{"name":"Institute for Clinical and Molecular Virology, University of Erlangen-Nuremberg, Erlangen, 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