Miura Kenji, Lee Jiyoung, Gong Qingqiu, Ma Shisong, Jin Jing Bo, Yoo Chan Yul, Miura Tomoko, Sato Aiko, Bohnert Hans J, Hasegawa Paul M
Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba 305-8572, Japan.
Plant Physiol. 2011 Feb;155(2):1000-12. doi: 10.1104/pp.110.165191. Epub 2010 Dec 14.
Phosphate (Pi) limitation causes plants to modulate the architecture of their root systems to facilitate the acquisition of Pi. Previously, we reported that the Arabidopsis (Arabidopsis thaliana) SUMO E3 ligase SIZ1 regulates root architecture remodeling in response to Pi limitation; namely, the siz1 mutations cause the inhibition of primary root (PR) elongation and the promotion of lateral root (LR) formation. Here, we present evidence that SIZ1 is involved in the negative regulation of auxin patterning to modulate root system architecture in response to Pi starvation. The siz1 mutations caused greater PR growth inhibition and LR development of seedlings in response to Pi limitation. Similar root phenotypes occurred if Pi-deficient wild-type seedlings were supplemented with auxin. N-1-Naphthylphthalamic acid, an inhibitor of auxin efflux activity, reduced the Pi starvation-induced LR root formation of siz1 seedlings to a level equivalent to that seen in the wild type. Monitoring of the auxin-responsive reporter DR5::uidA indicated that auxin accumulates in PR tips at early stages of the Pi starvation response. Subsequently, DR5::uidA expression was observed in the LR primordia, which was associated with LR elongation. The time-sequential patterning of DR5::uidA expression occurred earlier in the roots of siz1 as compared with the wild type. In addition, microarray analysis revealed that several other auxin-responsive genes, including genes involved in cell wall loosening and biosynthesis, were up-regulated in siz1 relative to wild-type seedlings in response to Pi starvation. Together, these results suggest that SIZ1 negatively regulates Pi starvation-induced root architecture remodeling through the control of auxin patterning.
磷酸盐（Pi）限制会导致植物调节其根系结构，以促进Pi的获取。此前，我们报道拟南芥（Arabidopsis thaliana）的SUMO E3连接酶SIZ1可响应Pi限制调节根系结构重塑；也就是说，siz1突变会导致主根（PR）伸长受到抑制，侧根（LR）形成增加。在此，我们提供证据表明，SIZ1参与生长素模式的负调控，以响应Pi饥饿调节根系结构。siz1突变导致幼苗在Pi限制条件下主根生长受到更大抑制，侧根发育增加。如果给缺Pi的野生型幼苗补充生长素，也会出现类似的根表型。生长素外排活性抑制剂N-1-萘基邻苯二甲酸（N-1-Naphthylphthalamic acid）可将Pi饥饿诱导的siz1幼苗侧根形成减少到与野生型相当的水平。对生长素响应报告基因DR5::uidA的监测表明，在Pi饥饿响应的早期阶段，生长素在主根根尖积累。随后，在侧根原基中观察到DR5::uidA表达，这与侧根伸长相关。与野生型相比，siz1根中DR5::uidA表达的时间顺序模式出现得更早。此外，微阵列分析显示，在响应Pi饥饿时，相对于野生型幼苗，siz1中其他几个生长素响应基因，包括参与细胞壁松弛和生物合成的基因，上调表达。总之，这些结果表明，SIZ1通过控制生长素模式对Pi饥饿诱导的根系结构重塑起负调控作用。
