Precise regulation of transcription termination is essential to cellular growthand survival. While premature stopping of transcription may produce truncated anddefective transcripts; stopping too late may disrupt the regulation of downstreamgenes in the same orientation and generate antisense RNA against genes in theopposite orientation. Either outcome would have significant impact on geneexpression. Thus, it is not surprising that transcription termination defects are causallyassociated with various human diseases, such as thrombophilia, thalassemia and cancer. We have previously demonstrated in a recent study that the mRNAcap-binding protein complex functions in conjunction with antitermination factor Npl3pto regulate transcription termination. In this project, I will continue to shed light on themechanisms of eukaryotic transcription termination in the model organism of buddingyeast using a combination of genetic and molecular biological methods. My study willfocus on the regulation of eukaryotic transcription termination through Npl3p and thefunctional coupling of eukaryotic transcription termination with RNA surveillance. Forthe first part, I will define the influence of post-translational modification of Npl3p on itsantitermination activity. For the second part, I will explore how cellular machineries oftranscription termination and RNA surveillance are functionally coupled with eachother. Particularly, I will investigate cotranscriptional recruitment of nuclear exosomeRrp6p. Because of the fundamental importance of transcription termination and highdegree of conservation of transcription termination machineries from yeast to human, our findings will have important implications in human diseases caused bytranscription termination defects.