The paracaspase MALT1 mediates T cell antigen receptor-induced signaling to the transcription factor NF-kappaB and is indispensable for T cell activation and proliferation. Enhanced expression of MALT1 or aberrant expression of a fusion protein of the apoptosis inhibitor API2 and MALT1 has been linked to mucosa-associated lymphoid tissue lymphoma. Despite the presence of a caspase-like domain, MALT1 proteolytic activity has not yet been demonstrated. Here we show that T cell antigen receptor stimulation induced recruitment of the NF-kappaB inhibitor A20 into a complex of MALT1 and the adaptor protein Bcl-10, leading to MALT1-mediated processing of A20. API2-MALT1 expression likewise resulted in cleavage of A20. MALT1 cleaved human A20 after arginine 439 and impaired its NF-kappaB-inhibitory function. Our studies identify A20 as a substrate of MALT1 and emphasize the importance of MALT1 proteolytic activity in the 'fine tuning' of T cell antigen receptor signaling.

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Ethylene inhibits hypocotyl elongation in etiolated Arabidopsis seedlings. However, when Arabidopsis was grown in the light in the presence of ethylene or its precursor 1-aminocyclopropane-1-carboxylic acid (ACC), a marked induction of hypocotyl elongation occurred. This resulted from an increase in cell expansion rather than cell division. The effects of ethylene and ACC were antagonized by the ethylene action inhibitor Ag ؉ . The elongation response was absent or weakened in a set of ethylene-insensitive mutants (etr1-3, ein2-1, ein3-1, ein4, ain1-10, ein7). With the exception of ein4, the degree of inhibition of hypocotyl elongation was correlated with the strength of the ethylene-insensitive phenotype based on the triple response assay. In addition, the constitutive ethylene response mutant ctr1-1, grown in the light, had a longer hypocotyl than the wild type. Exogenous auxin also induced hypocotyl elongation in light-grown Arabidopsis. Again, the response was abolished by treatment with Ag ؉ , suggesting that ethylene might be a mediator. The results showed that, depending on light conditions, ethylene can induce opposite effects on cell expansion in Arabidopsis hypocotyls.Plant cell expansion is thought to be controlled by the orientation of cortical microtubules in combination with both the extensibility of the cell wall and the turgor pressure inside the cell (1, 2). These processes are under control of light and phytohormones. Ethylene can both promote and inhibit cell growth depending on plant species and cell type (3). In Arabidopsis, it was found to inhibit cell expansion (4, 5). Hence, Arabidopsis plants treated with ethylene, as well as a mutant displaying constitutive ethylene responses (ctr1), show a severe growth inhibition throughout development. Roots and inflorescences are short and leaves remain unexpanded. In etiolated Arabidopsis seedlings, ethylene prevents hypocotyl elongation (6). Recently, with the cloning and characterization of the Arabidopsis HOOKLESS1 (HLS1) gene, it has been shown that ethylene can also promote cell elongation (7). Specific cells in the apical hook of etiolated seedlings are induced to elongate with differential growth and hook curvature as a result. HLS1 is thought to control growth via regulation of transport or chemical modification of auxin. Other examples of a cross-talk between the ethylene and auxin pathways have been found. Most auxin-resistant mutants appeared to be also ethylene insensitive (8). Moreover, studies with aux1 suggested that ethylene sensitivity is regulated by auxin (9). Current molecular-genetic approaches shed a new light on previous physiological evidence for a complex interplay between these two hormones (10, 11).Most ethylene mutants in Arabidopsis have been identified using the triple response (12). Analysis of the ethyleneinsensitive mutants etr1 (6), ein2 (13), and ain1 (14) demonstrated that the effects of this class of mutations are not restricted to the etiolated seedling stage, but are also observed throughout the life c...