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J. Biol. Chem., Vol. 275, Issue 29, 22136-22146, July 21, 2000
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From the Mcl-1 is a member of the Bcl-2 family that is
regulated transcriptionally and post-transcriptionally, with expression
of the full-length Mcl-1-encoded gene product resulting in enhanced
cell survival. As reported here, the human Mcl-1 gene can also undergo differential splicing, which yields an internally deleted,
death-inducing gene product,
Mcl-1s/ The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF198614.
Exon Skipping in Mcl-1 Results in a Bcl-2 Homology Domain 3 Only
Gene Product That Promotes Cell Death*
§,,,
Respiratory Cell and Molecular Biology
Laboratory, Division of Molecular and Genetic Medicine, The University
of Sheffield Medical School, Sheffield, S10 2RX, United Kingdom and
the ¶ Department of Pharmacology and Toxicology, Dartmouth Medical
School, Hanover, New Hampshire 03755-3835
TM. Whereas full-length Mcl-1
derives from three coding exons (instead of the two present in Bcl-2
and other anti-apoptotic members of this family), the
Mcl-1s/TM splice variant results from the
joining of the first and third exons with skipping of the central exon.
Because of the skipped exon and a shift in the reading frame
downstream, the Bcl-2 homology domain (BH3) remains intact, whereas the
BH1-, BH2-, and transmembrane-encoding domains do not.
Mcl-1s/TM thus has features similar to BH3 only, pro-apoptotic Bcl-2 family members and, accordingly, was found to
promote cell death. In addition to a variety of other types of
regulation, the Mcl-1 gene appears ideally designed for the generation
of either a Bcl-2-like viability promoting or, as reported here, a BH3
only death-inducing gene product.
*
This work was supported by grants from the Special Trustees
for the Former United Sheffield Hospitals and Grant CA57359 from the
National Institutes of Health.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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