scholarly journals mRNA export through an additional cap-binding complex consisting of NCBP1 and NCBP3

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Anna Gebhardt ◽  
Matthias Habjan ◽  
Christian Benda ◽  
Arno Meiler ◽  
Darya A. Haas ◽  
...  
2007 ◽  
Vol 282 (21) ◽  
pp. 15645-15651 ◽  
Author(s):  
Takayuki Nojima ◽  
Tetsuro Hirose ◽  
Hiroshi Kimura ◽  
Masatoshi Hagiwara

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Rwik Sen ◽  
Priyanka Barman ◽  
Amala Kaja ◽  
Jannatul Ferdoush ◽  
Shweta Lahudkar ◽  
...  

ABSTRACTCap-binding complex (CBC) associates cotranscriptionally with the cap structure at the 5′ end of nascent mRNA to protect it from exonucleolytic degradation. Here, we show that CBC promotes the targeting of an mRNA export adaptor, Yra1 (forming transcription export [TREX] complex with THO and Sub2), to the active genes and enhances mRNA export inSaccharomyces cerevisiae. Likewise, recruitment of Npl3 (an hnRNP involved in mRNA export via formation of export-competent ribonuclear protein complex [RNP]) to the active genes is facilitated by CBC. Thus, CBC enhances targeting of the export factors and promotes mRNA export. Such function of CBC is not mediated via THO and Sub2 of TREX, cleavage and polyadenylation factors, or Sus1 (that regulates mRNA export via transcription export 2 [TREX-2]). However, CBC promotes splicing ofSUS1mRNA and, consequently, Sus1 protein level and mRNA export via TREX-2. Collectively, our results support the hypothesis that CBC promotes recruitment of Yra1 and Npl3 to the active genes, independently of THO, Sub2, or cleavage and polyadenylation factors, and enhances mRNA export via TREX and RNP, respectively, in addition to its role in facilitatingSUS1mRNA splicing to increase mRNA export through TREX-2, revealing distinct stimulatory functions of CBC in mRNA export.


2000 ◽  
Vol 20 (8) ◽  
pp. 2827-2838 ◽  
Author(s):  
Biswadip Das ◽  
Zijian Guo ◽  
Patrick Russo ◽  
Pascal Chartrand ◽  
Fred Sherman

ABSTRACT The cyc1-512 mutation in Saccharomyces cerevisiae causes a 90% reduction in the level of iso-1-cytochrome c because of the lack of a proper 3′-end-forming signal, resulting in low levels of eight aberrantly longcyc1-512 mRNAs which differ in length at their 3′ termini. cyc1-512 can be suppressed by deletion of either of the nonessential genes CBC1 and CBC2, which encode the CBP80 and CBP20 subunits of the nuclear cap binding complex, respectively, or by deletion of the nonessential gene UPF1, which encodes a major component of the mRNA surveillance complex. The upf1-Δ deletion suppressed the cyc1-512defect by diminishing degradation of the longer subset ofcyc1-512 mRNAs, suggesting that downstream elements or structures occurred in the extended 3′ region, similar to the downstream elements exposed by transcripts bearing premature nonsense mutations. On the other hand, suppression of cyc1-512defects by cbc1-Δ occurred by two different mechanisms. The levels of the shorter cyc1-512 transcripts were enhanced in the cbc1-Δ mutants by promoting 3′-end formation at otherwise-weak sites, whereas the levels of the longercyc1-512 transcripts, as well as of all mRNAs, were slightly enhanced by diminishing degradation. Furthermore,cbc1-Δ greatly suppressed the degradation of mRNAs and other phenotypes of a rat7-1 strain which is defective in mRNA export. We suggest that Cbc1p defines a novel degradation pathway that acts on mRNAs partially retained in nuclei.


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