Gaczynska M, Goldberg A L, Tanaka K, Hendil K B, Rock K L
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Biol Chem. 1996 Jul 19;271(29):17275-80. doi: 10.1074/jbc.271.29.17275.
Most antigenic peptides presented on major histocompatibility complex class I molecules are generated by proteasomes. Interferon-gamma, which stimulates antigen presentation, induces new proteasome beta-subunits LMP2 and LMP7, which replace the homologous beta-subunits Y (delta) and X (epsilon). As a result, the capacity of the proteasome to cleave model peptides increases after hydrophobic and basic residues and falls after acidic residues. To clarify the function of these subunits, we examined the effects of overexpressing subunits X (delta) and Y (epsilon). Transfection of the Y gene into HeLa cells stimulated the proteasomal cleavage after acidic residues without altering other peptidase activities. This effect was proportional to the amount of the Y subunits and opposite to the effect of its homolog, LMP2. Y appears to promote cleavages after acidic residues. Furthermore, in mutants lacking the LMP genes (in contrast to wild-type cells), interferon-gamma treatment increased the proteasome content of Y subunits and enhanced postacidic cleavages. Transfection with cDNA for the X subunit reduced hydrolysis after hydrophobic and basic residues, an effect opposite to transfection of LMP2 and LMP7. Surprisingly, transfection of X increased the amounts not only of X, but also of Y, while decreasing LMP2 content. Thus, the loss of the Y subunit upon interferon-gamma treatment or LMP2 transfection accounts for the suppression of postacidic cleavages, and the loss of X contributes to the increased hydrolysis after hydrophobic and basic residues. These adaptations should favor the production of the kinds of peptides that are presented on major histocompatibility complex class I molecules.
大多数呈递于主要组织相容性复合体I类分子上的抗原肽是由蛋白酶体产生的。刺激抗原呈递的γ干扰素可诱导新的蛋白酶体β亚基LMP2和LMP7的产生,它们会取代同源的β亚基Y(δ)和X(ε)。结果,蛋白酶体切割模型肽的能力在疏水和碱性残基后增强,而在酸性残基后减弱。为了阐明这些亚基的功能,我们研究了过表达亚基X(δ)和Y(ε)的影响。将Y基因转染到HeLa细胞中可刺激酸性残基后的蛋白酶体切割,而不改变其他肽酶活性。这种效应与Y亚基的量成正比,且与其同源物LMP2的效应相反。Y似乎促进酸性残基后的切割。此外,在缺乏LMP基因的突变体中(与野生型细胞相反),γ干扰素处理增加了Y亚基的蛋白酶体含量并增强了酸性后切割。用X亚基的cDNA转染可减少疏水和碱性残基后的水解,这一效应与转染LMP2和LMP7相反。令人惊讶的是,转染X不仅增加了X的量,还增加了Y的量,同时降低了LMP2的含量。因此,γ干扰素处理或LMP2转染后Y亚基的缺失导致了酸性后切割的抑制,而X的缺失则导致了疏水和碱性残基后水解的增加。这些适应性变化应有利于产生呈递于主要组织相容性复合体I类分子上的各类肽。