Identification of a novel E3 ubiquitin ligase that is required for suppression of premature senescence in Arabidopsis Export

@article{citeulike:5007040, abstract = {During leaf senescence, resources are recycled by redistribution to younger leaves and reproductive organs. Candidate pathways for the regulation of onset and progression of leaf senescence include ubiquitin-dependent turnover of key proteins. Here, we identified a novel plant U-box E3 ubiquitin ligase that prevents premature senescence in Arabidopsis plants, and named it SENESCENCE-ASSOCIATED E3 UBIQUITIN LIGASE 1 (SAUL1). Using in vitro ubiquitination assays, we show that SAUL1 has E3 ubiquitin ligase activity. We isolated two alleles of saul1 mutants that show premature senescence under low light conditions. The visible yellowing of leaves is accompanied by reduced chlorophyll content, decreased photochemical efficiency of photosystem II and increased expression of senescence genes. In addition, saul1 mutants exhibit enhanced abscisic acid (ABA) biosynthesis. We show that application of ABA to Arabidopsis is sufficient to trigger leaf senescence, and that this response is abolished in the ABA-insensitive mutants abi1-1 and abi2-1, but enhanced in the ABA-hypersensitive mutant era1-3. We found that increased ABA levels coincide with enhanced activity of Arabidopsis aldehyde oxidase 3 (AAO3) and accumulation of AAO3 protein in saul1 mutants. Using label transfer experiments, we showed that interactions between SAUL1 and AAO3 occur. This suggests that SAUL1 participates in targeting AAO3 for ubiquitin-dependent degradation via the 26S proteasome to prevent premature senescence.}, address = {Molekulare Pflanzenphysiologie, Friedrich-Alexander-Universitt Erlangen-Nrnberg, Staudtstrasse 5, D-91058 Erlangen, Germany; Institut fr Pflanzenbiologie, Technische Universitt Braunschweig, Spielmannstrasse 7, D-38106 Braunschweig, Germany; Julius-von-Sachs-Institut fr Biowissenschaften, Universitt Wrzburg, Julius-von-Sachs-Platz 2, D-97082 Wrzburg, Germany; Department of Biological Sciences, Tokyo Metropolitan University, Hachioji, Tokyo 192-0397, Japan}, author = {Raab, Sabine and Drechsel, Gabriele and Zarepour, Maryam and Hartung, Wolfram and Koshiba, Tomokazu and Bittner, Florian and Hoth, Stefan}, citeulike-article-id = {5007040}, citeulike-linkout-0 = {http://dx.doi.org/10.1111/j.1365-313X.2009.03846.x}, citeulike-linkout-1 = {http://www.ingentaconnect.com/content/bsc/tpj/2009/00000059/00000001/art00004}, citeulike-linkout-2 = {http://www3.interscience.wiley.com/cgi-bin/abstract/122219871/ABSTRACT}, doi = {10.1111/j.1365-313X.2009.03846.x}, issn = {1365-313X}, journal = {The Plant Journal}, keywords = {aba, senescence}, number = {1}, pages = {39--51}, posted-at = {2009-09-28 12:21:13}, priority = {2}, publisher = {Blackwell Publishing}, title = {Identification of a novel E3 ubiquitin ligase that is required for suppression of premature senescence in Arabidopsis}, url = {http://dx.doi.org/10.1111/j.1365-313X.2009.03846.x}, volume = {59}, year = {2009} }

TY - JOUR ID - citeulike:5007040 L3 - citeulike-article-id:5007040 N2 - During leaf senescence, resources are recycled by redistribution to younger leaves and reproductive organs. Candidate pathways for the regulation of onset and progression of leaf senescence include ubiquitin-dependent turnover of key proteins. Here, we identified a novel plant U-box E3 ubiquitin ligase that prevents premature senescence in Arabidopsis plants, and named it SENESCENCE-ASSOCIATED E3 UBIQUITIN LIGASE 1 (SAUL1). Using in vitro ubiquitination assays, we show that SAUL1 has E3 ubiquitin ligase activity. We isolated two alleles of saul1 mutants that show premature senescence under low light conditions. The visible yellowing of leaves is accompanied by reduced chlorophyll content, decreased photochemical efficiency of photosystem II and increased expression of senescence genes. In addition, saul1 mutants exhibit enhanced abscisic acid (ABA) biosynthesis. We show that application of ABA to Arabidopsis is sufficient to trigger leaf senescence, and that this response is abolished in the ABA-insensitive mutants abi1-1 and abi2-1, but enhanced in the ABA-hypersensitive mutant era1-3. We found that increased ABA levels coincide with enhanced activity of Arabidopsis aldehyde oxidase 3 (AAO3) and accumulation of AAO3 protein in saul1 mutants. Using label transfer experiments, we showed that interactions between SAUL1 and AAO3 occur. This suggests that SAUL1 participates in targeting AAO3 for ubiquitin-dependent degradation via the 26S proteasome to prevent premature senescence. IS - 1 JF - The Plant Journal SN - 1365-313X AD - Molekulare Pflanzenphysiologie, Friedrich-Alexander-Universitt Erlangen-Nrnberg, Staudtstrasse 5, D-91058 Erlangen, Germany; Institut fr Pflanzenbiologie, Technische Universitt Braunschweig, Spielmannstrasse 7, D-38106 Braunschweig, Germany; Julius-von-Sachs-Institut fr Biowissenschaften, Universitt Wrzburg, Julius-von-Sachs-Platz 2, D-97082 Wrzburg, Germany; Department of Biological Sciences, Tokyo Metropolitan University, Hachioji, Tokyo 192-0397, Japan EP - 51 TI - Identification of a novel E3 ubiquitin ligase that is required for suppression of premature senescence in Arabidopsis PB - Blackwell Publishing VL - 59 SP - 39 KW - aba KW - senescence AU - Raab, Sabine AU - Drechsel, Gabriele AU - Zarepour, Maryam AU - Hartung, Wolfram AU - Koshiba, Tomokazu AU - Bittner, Florian AU - Hoth, Stefan PY - 2009/// UR - http://dx.doi.org/10.1111/j.1365-313X.2009.03846.x ER -