Jin Jing Bo, Jin Yin Hua, Lee Jiyoung, Miura Kenji, Yoo Chan Yul, Kim Woe-Yeon, Van Oosten Michael, Hyun Youbong, Somers David E, Lee Ilha, Yun Dae-Jin, Bressan Ray A, Hasegawa Paul M
Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, IN 47907 2010, USA.
Plant J. 2008 Feb;53(3):530-40. doi: 10.1111/j.1365-313X.2007.03359.x. Epub 2007 Dec 6.
Loss-of-function siz1 mutations caused early flowering under short days. siz1 plants have elevated salicylic acid (SA) levels, which are restored to wild-type levels by expressing nahG, bacterial salicylate hydroxylase. The early flowering of siz1 was suppressed by expressing nahG, indicating that SIZ1 represses the transition to flowering mainly through suppressing SA-dependent floral promotion signaling under short days. Previous results have shown that exogenous SA treatment does not suppress late flowering of autonomous pathway mutants. However, the siz1 mutation accelerated flowering time of an autonomous pathway mutant, luminidependens, by reducing the expression of FLOWERING LOCUS C (FLC), a floral repressor. This result suggests that SIZ1 promotes FLC expression, possibly through an SA-independent pathway. Evidence indicates that SIZ1 is required for the full activation of FLC expression in the late-flowering FRIGIDA background. Interestingly, increased FLC expression and late flowering of an autonomous pathway mutant, flowering locus d (fld), was not suppressed by siz1, suggesting that SIZ1 promotes FLC expression by repressing FLD. Consistent with this, SIZ1 facilitates sumoylation of FLD that can be suppressed by mutations in three predicted sumoylation motifs in FLD (i.e. FLDK3R). Furthermore, expression of FLDK3R in fld protoplasts strongly reduced FLC transcription compared with expression of FLD, and this affect was linked to reduced acetylation of histone 4 in FLC chromatin. Taken together, the results suggest that SIZ1 is a floral repressor that not only represses the SA-dependent pathway, but also promotes FLC expression by repressing FLD activity through sumoylation, which is required for full FLC expression in a FRIGIDA background.
功能丧失型siz1突变导致短日条件下早花。siz1植株的水杨酸（SA）水平升高，通过表达细菌水杨酸羟化酶nahG可将其恢复到野生型水平。nahG的表达抑制了siz1的早花现象，表明SIZ1在短日条件下主要通过抑制SA依赖的促进开花信号来抑制开花转变。先前的研究结果表明，外源SA处理不能抑制自主途径突变体的晚花现象。然而，siz1突变通过降低开花抑制因子开花位点C（FLC）的表达，加速了自主途径突变体luminidependens的开花时间。这一结果表明，SIZ1可能通过一条不依赖SA的途径促进FLC的表达。有证据表明，在晚花的FRIGIDA背景中，FLC表达的完全激活需要SIZ1。有趣的是，siz1并未抑制自主途径突变体开花位点d（fld）中FLC表达的增加和晚花现象，这表明SIZ1通过抑制FLD来促进FLC的表达。与此一致的是，SIZ1促进FLD的SUMO化，而FLD中三个预测的SUMO化基序（即FLDK3R）的突变可抑制这种SUMO化。此外，与FLD的表达相比，FLDK3R在fld原生质体中的表达显著降低了FLC的转录，这种影响与FLC染色质中组蛋白4乙酰化的减少有关。综上所述，这些结果表明，SIZ1是一种开花抑制因子，它不仅抑制SA依赖的途径，还通过SUMO化抑制FLD活性来促进FLC的表达，而这在FRIGIDA背景中是FLC完全表达所必需的。
