Armengot Laia, Marquès-Bueno María Mar, Soria-Garcia Angel, Müller Maren, Munné-Bosch Sergi, Martínez María Carmen
Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, 08193, Bellaterra (Barcelona), Spain.
Plant J. 2014 May;78(3):411-23. doi: 10.1111/tpj.12481. Epub 2014 Apr 2.
We have previously reported that CK2-defective Arabidopsis thaliana plants (CK2mut plants) were impaired severely in root development and auxin polar transport, and exhibited transcriptional misregulation of auxin-efflux transporters (Plant J., 67, 2011a, 169). In this work we show that CK2mut roots accumulate high levels of salicylic acid (SA) and that the gene that encodes isochorismate synthase (SID2) is overexpressed, strongly suggesting that CK2 activity is required for SA biosynthesis via the shikimate pathway. Moreover, SA activates transcription of CK2-encoding genes and, thus, SA and CK2 appear to be part of an autoregulatory feed-back loop to fine-tune each other's activities. We also show that exogenous SA and constitutive high SA levels in cpr mutants reproduce the CK2mut root phenotypes (decrease of root length and of number of lateral roots), whereas inhibition of CK2 activity in SA-defective and SA-signalling mutants lead to less severe phenotypes, suggesting that the CK2mut root phenotypes are SA-mediated effects. Moreover, exogenous SA mediates transcriptional repression of most of PIN-FORMED (PIN) genes, which is the opposite effect observed in CK2mut roots. These results prompted us to propose a model in which CK2 acts as a link between SA homeostasis and transcriptional regulation of auxin-efflux transporters. We also show that CK2 overexpression in Arabidopsis has neither impact on SA biosynthesis nor on auxin transport, but it improves the Arabidopsis root system. Thus, unlike the outcome in mammals, an excess of CK2 in plant cells does not produce neoplasia, but it might be advantageous for plant fitness.
我们之前报道过，缺乏CK2的拟南芥植株（CK2mut植株）在根系发育和生长素极性运输方面严重受损，并表现出生长素外排转运蛋白的转录失调（《植物杂志》，67卷，2011年a期，169页）。在这项研究中，我们发现CK2mut根系积累了高水平的水杨酸（SA），并且编码异分支酸合酶（SID2）的基因过度表达，这强烈表明CK2活性是通过莽草酸途径进行SA生物合成所必需的。此外，SA激活编码CK2的基因的转录，因此，SA和CK2似乎是一个自动调节反馈环的一部分，以相互微调彼此的活性。我们还表明，外源SA和cpr突变体中组成型高SA水平重现了CK2mut根系表型（根长度和侧根数量减少），而在SA缺陷和SA信号突变体中抑制CK2活性导致的表型较轻，这表明CK2mut根系表型是SA介导的效应。此外，外源SA介导了大多数PIN-FORMED（PIN）基因的转录抑制，这与在CK2mut根系中观察到的相反效应。这些结果促使我们提出一个模型，其中CK2作为SA稳态和生长素外排转运蛋白转录调控之间的联系。我们还表明，拟南芥中CK2的过表达对SA生物合成和生长素运输均无影响，但它改善了拟南芥的根系系统。因此，与哺乳动物中的结果不同，植物细胞中过量的CK2不会产生肿瘤形成，但它可能对植物适应性有利。
