New way of regulating alternative splicing in retroviruses: the promoter makes a difference.
Alternative splicing has been recognized as a major mechanism for creating proteomic diversity from a limited number of genes. However, not all determinants regulating this process have been characterized. Using subviral human immunodeficiency virus (HIV) env constructs we observed an enhanced splicing of the RNA when expression was under control of the cytomegalovirus (CMV) promoter instead of the HIV long terminal repeat (LTR). We extended these observations to LTR- or CMV-driven murine leukemia proviruses, suggesting that retroviral LTRs are adapted to inefficient alternative splicing at most sites in order to maintain balanced gene expression.
Bohne
Jens
J
Experimental Hematology, Hannover Medical School, Carl-Neuberg-Strasse 1, OE 6960, D-30625 Hanover, Germany. bohne.jens@mh-hannover.de
Schambach
Axel
A
Zychlinski
Daniela
D
D017398:Alternative Splicing / Q000235:genetics*; D003587:Cytomegalovirus / Q000235:genetics; D015696:Gene Products, tat / Q000235:genetics / Q000378:metabolism; D006678:HIV / Q000235:genetics* / Q000378:metabolism; D016325:HIV Long Terminal Repeat; D009052:Leukemia Virus, Murine / Q000235:genetics* / Q000378:metabolism; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012367:RNA, Viral / Q000235:genetics; D014759:Viral Envelope Proteins / Q000235:genetics / Q000378:metabolism; D054322:tat Gene Products, Human Immunodeficiency Virus
D015696:Gene Products, tat; D012367:RNA, Viral; D014759:Viral Envelope Proteins; D054322:tat Gene Products, Human Immunodeficiency Virus