Quon Tezz, Lampugnani Edwin R, Smyth David R
School of Biological Sciences, Monash University, Clayton VIC, Australia.
Front Plant Sci. 2017 Feb 8;8:152. doi: 10.3389/fpls.2017.00152. eCollection 2017.
The activity of genes controlling organ development may be associated with the redox state of subregions within the meristem. Glutaredoxins react to the level of oxidative potential and can reduce cysteine dithiols, in some cases to activate specific transcription factors. In Arabidopsis, loss of function of the glutaredoxin ROXY1 or the trihelix transcription factor PETAL LOSS (PTL) each results in reduced numbers of petals. Here, genetic studies have revealed that loss of petals in mutant plants depends on ROXY1 function. The two genes also act together to restrain stamen-identifying C function from entering the outer whorls. On the other hand, they suppress growth between sepals and in sepal margins, with ROXY1 action partially redundant to that of PTL. Genetic interactions with mutations indicate that auxin activity is reduced in the petal whorl of mutants as in mutants. However, it is apparently increased in the sepal whorl of triple mutants associated with the ectopic outgrowth of sepal margins, and of finger-like extensions of inter-sepal zones that in 20% of cases are topped with bunches of ectopic sepals. These interactions may be indirect, although PTL and ROXY1 proteins can interact directly when co-expressed in a transient assay. Changes of conserved cysteines within PTL to similar amino acids that cannot be oxidized did not block its function. It may be in some cases that under reducing conditions ROXY1 binds PTL and activates it by reducing specific conserved cysteines, thus resulting in growth suppression.
控制器官发育的基因活性可能与分生组织内亚区域的氧化还原状态有关。谷氧还蛋白对氧化电位水平作出反应,并能还原半胱氨酸二硫醇,在某些情况下可激活特定的转录因子。在拟南芥中,谷氧还蛋白ROXY1或三螺旋转录因子花瓣缺失(PTL)功能丧失均会导致花瓣数量减少。在此,遗传学研究表明突变植物中花瓣的缺失取决于ROXY1的功能。这两个基因还共同作用,抑制决定雄蕊的C功能进入外层轮。另一方面,它们抑制萼片之间和萼片边缘的生长,ROXY1的作用与PTL的作用部分冗余。与突变的遗传相互作用表明,与突变体一样,突变体花瓣轮中的生长素活性降低。然而,在与萼片边缘异位生长以及萼片间区域指状延伸相关的三突变体的萼片轮中,生长素活性明显增加,在20%的情况下,这些延伸顶端有一束束异位萼片。这些相互作用可能是间接的,尽管PTL和ROXY1蛋白在瞬时检测中共表达时可以直接相互作用。将PTL中保守的半胱氨酸突变为不能被氧化的类似氨基酸并没有阻断其功能。在某些情况下,可能是在还原条件下,ROXY1与PTL结合并通过还原特定的保守半胱氨酸来激活它,从而导致生长抑制。