Post-splicing intron RNA degradation is thought to serve several
purposes, including recycling of splicing factors and minimizing reverse
splicing. Unlike excised intron RNAs of spliceosomal and group I introns
which are degraded efficiently in vivo, excised group II intron
RNA lariats accumulate in yeast mitochondria. We are investigating two
in vivo situations in which the relatively stable excised group II
intron RNAs are degraded efficiently. Many transformed mutations of
intron 5gamma of the COXI gene of yeast mtDNA, or their
revertants, permit some splicing with efficient branching
( e.g., Boulanger et al., MCB [1995] 15, 4479-4488).
Unexpectedly, in most of those mutant strains, the resulting
lariat RNAs are substantially degraded. Disruption of the nuclear
DBR1 gene, which encodes the Dbr1p nuclear lariat debranching
enzyme, has no effect on the level of splicing in those strains, but
stabilizes the mutant lariat RNAs ~10-fold. Thus, Dbr1p may be present
in mitochondria and may play a direct role in the post-splicing
metabolism of group II intron RNA lariats. Also, excised linear
group II intron RNAs that result from splicing by first step hydrolysis
(see Podar et al., Nature [1998] 391, 915-918) are degraded
efficiently in vivo. These linear RNAs remain unstable in a
deltadbr1 strain, and also in a deltanuc1 strain that lacks
a known mitochondrial nuclease. Mutation or disruption of the
SUV3 gene, which encodes an essential subunit of an enzyme that
degrades linear group I intron RNAs, does not stabilize the linear group
II intron RNAs. Thus, efficient degradation of linear group II intron
RNAs depends on other enzymes.
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