𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Alternative modes of mRNA processing in a 3′ splice site mutant ofNeurospora crassa

✍ Scribed by Jane H. Kinnaird; Dean F. Revell; Ian F. Connerton; Isobelle Hasleham; John R. S. Fincham

Book ID
104735457
Publisher
Springer-Verlag
Year
1992
Tongue
English
Weight
737 KB
Volume
22
Category
Article
ISSN
0172-8083

No coin nor oath required. For personal study only.

✦ Synopsis

The am s mutant of Neurospora crassa is shown to have a double base-pair change, GTG for the normal TAG, at the 3' end of the second intron of the am (NADP-specific glutamate dehydrogenase, GDH) gene. The greater part of the mutant am transcript accumulates as two fragments hybridising to probes for sequences respectively upstream and downstream of the 5' e~d of the intron. Two processed transcripts approximating to normal full length mRNA were identified. In one the second intron was intact; in the other the second intron was spliced out through the use of an AAG sequence, 20 base-pairs into the third exon, as a 3' acceptor site. A GAG sequence, only four base-pairs downstream from the normal acceptor site, does not appear to be used.

📜 SIMILAR VOLUMES

A novel splice-acceptor site mutation (I
A novel splice-acceptor site mutation (IVS13-2A>T) of polycystic kidney disease 1 (PKD1) gene resulting in an RNA processing defect with a 74-nucleotide deletion in exon 14 of the mRNA transcript
✍ Anna Thongnoppakhun; Nanyawan Rungroj; Prapon Wilairat; Kriengsak Vareesangthip; 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 222 KB 👁 3 views

Autosomal dominant polycystic kidney disease (ADPKD) occurs mainly from mutations of polycystic kidney disease 1 (PKD1) gene. A novel mutation of the PKD1 gene due to a nucleotide substitution in splice-acceptor site of IVS13 (AG->TG) was identified by analyses of PKD1-cDNA and genomic DNA. The IVS1

An activated 5′ cryptic splice site in t
An activated 5′ cryptic splice site in the human ALG3 gene generates a premature termination codon insensitive to nonsense-mediated mRNA decay in a new case of congenital disorder of glycosylation type Id (CDG-Id)
✍ Jonas Denecke; Christian Kranz; Dirk Kemming; Hans-Georg Koch; Thorsten Marquard 📂 Article 📅 2004 🏛 John Wiley and Sons 🌐 English ⚖ 305 KB

A defect of the dolichyl-P-Man:Man5GlcNAc2-PP-dolichyl mannosyltransferase encoded by the ALG3 gene (alias NOT56L) causes congenital disorder of glycosylation type Id (CDG-Id). In this work, a new mutation in the ALG3 gene causing atypical splicing is described with characterization of expression le