MCL-1ES, a novel variant of MCL-1, associates with MCL-1L and induces mitochondrial cell death

Myeloid cell leukemia-1 (MCL-1L) is a pro-survival member of the BCL-2 family that promotes cell survival. In this study, we identify a new splicing variant of human MCL-1 that encodes MCL-1ES ( extra short). Sequence analysis indicates that this variant results from splicing within the first coding exon of MCL-1 at a non-canonical GC-AG donor-acceptor pair. The deduced sequence of MCL-1ES encodes a protein of 197 amino acids, and the PEST ( proline, glutamic acid, serine, and threonine) motifs present in MCL-1L are absent. MCL-1ES interacts with MCL-1L and induces mitochondrial cell death, suggesting that alternative splicing of MCL-1 may control the fate of cells. Structured summary: MINT-7255705, MINT-7255718, MINT-7255731, MINT-7255743: MCL1-ES (uniprotkb: Q07820-2) physically interacts (MI:0914) with MCL1-1L (uniprotkb: Q07820-1) by anti tag coimmunoprecipitation ( MI: 0007) MINT-7255771: MCL1-ES ( uniprotkb: Q07820-2) physically interacts (MI: 0914) with Beta actin ( uniprotkb: P60709) by anti tag coimmunoprecipitation ( MI: 0007) MINT-7255781: MCL1-ES ( uniprotkb: Q07820-2) physically interacts (MI: 0914) with GAPDH ( uniprotkb: P04406) by anti tag coimmunoprecipitation ( MI: 0007) MINT-7255756: MCL1-ES ( uniprotkb: Q07820-2) physically interacts (MI: 0914) with COX IV ( uniprotkb: P13073) by anti tag coimmunoprecipitation (MI: 0007) (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.