Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.31 (
beta-glucuronidase
)
7,680
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Either of the first two introns of the Arabidopsis tryptophan pathway gene
PAT1
elevates mRNA accumulation from a
PAT1
:
beta-glucuronidase
(GUS) fusion roughly 5-fold without affecting the rate of
PAT1
:GUS transcription. To further explore the mechanism of this intron-mediated enhancement of gene expression, we wanted to determine whether splicing or specific intron sequences were necessary. In-frame derivatives of
PAT1
intron 1, whose splicing was prevented by a point mutation or large deletions, were able to increase mRNA accumulation from a
PAT1
:GUS fusion, demonstrating that splicing per se is not required. Furthermore, each of a series of introns containing overlapping deletions that together span
PAT1
intron 1 increased
PAT1
:GUS mRNA accumulation as much as the full-length intron did, indicating that all intron sequences are individually dispensable for this phenomenon. These results eliminate the simple idea that this intron stimulates mRNA accumulation via a unique RNA-stabilizing sequence or through the completed act of splicing. However, they are consistent with a possible role for redundant intron sequence elements or an association of the pre-mRNA with the spliceosome.
...
PMID:Intron-mediated enhancement of gene expression independent of unique intron sequences and splicing. 1067 46