High impact information on NAB3

• The RNA-binding protein Nab3, the putative RNA helicase Sen1, and the intact C-terminal domain of pol II are also required for efficient response to the element [1].
• Yeast RNA binding proteins Nrd1 and Nab3 direct termination of sn/snoRNAs and recently have also been implicated in premature transcription termination of the NRD1 gene [2].
• Mutation of Nrd1 and Nab3 binding sites within the NRD1 mRNA leads to a relative increase in Pol II occupancy of downstream sequences [3].
• Our results suggest an important role for the Nrd1p-Nab3p pathway in the control of gene expression throughout the genome [4].
• We identified NAB3 as a dosage suppressor of rtf1 [5].

Biological context of NAB3

• The NAB3 gene is essential for cell viability and encodes an acidic ribonucleoprotein [6].
• Nrd1 and Nab3 colocalize to regions of the genome expressing antisense CUTs, and these transcripts require yeast nuclear exosome and TRAMP components for degradation [2].

Regulatory relationships of NAB3

• Temperature-sensitive alleles of NAB3 are suppressed by deletion of CTK1, a kinase that has been shown to phosphorylate the CTD and increase elongation efficiency in vitro [7].
• In this paper, we show that NRD1 expression is regulated by Nrd1- and Nab3-directed premature termination [3].

Other interactions of NAB3

• The present work demonstrates genetic and physical interactions among Nrd1p, the pol II CTD, Nab3p, and the CTD kinase CTDK-I [7].
• Nab1p, Nab2p, and Nab3p were isolated by a method which uses UV light to cross-link proteins directly bound to poly(A)+ RNA in vivo [6].
• Overproduction of HMD1 results in a relatively specific reduction in the level of the CLN3 or CLN3-2 transcript [8].

Analytical, diagnostic and therapeutic context of NAB3

• Dissection of a CUT terminator reveals a minimal element sufficient for Nrd1- and Nab3-directed termination [2].

References