Perturbation of lignin biosynthesis often results in severe growth and developmental defects in plants, which imposes practical limitations to genetic enhancement of lignocellulosic biomass for biofuel production. Currently, little information is known about the cellular and genetic mechanisms of this important phenomenon. Here we show that defects in both cell division and cell expansion underlie the dwarfism of an Arabidopsis lignin mutant ref8 , and report the identification of a GROWTH INHIBITION RELIEVED 1 (GIR1 ) gene from a suppressor screen. GIR1 encodes an importin‐beta‐like protein required for the nuclear import of MYB4, a transcriptional repressor of phenylpropanoid metabolism. Disruption of GIR1 and MYB4 similarly alleviates the cellular defects and growth inhibition in ref8 , suggesting that the growth rescue effect of gir1 is likely due to compromised MYB4 transport and function. Importantly, the phenylpropanoid perturbation is not alleviated in gir1 ref8 and myb4 ref8 , suggesting that the function of MYB4 in growth inhibition of lignin‐modified plants is likely to be distinct from its known role in transcriptional regulation of phenylpropanoid biosynthetic genes. This study also provides evidence that lignin‐modification‐induced dwarfism is not merely due to compromised water transport brought about by lignin deficiency, as gir1 has no effect on the growth inhibition of other lignin mutants that show the collapsed xylem phenotype.

中文翻译：

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Importin-beta样蛋白介导拟南芥中木质素修饰诱导的矮化。

木质素生物合成的扰动通常导致植物严重的生长和发育缺陷，这对木质纤维素生物质用于生物燃料生产的遗传增强施加了实际限制。目前，关于这种重要现象的细胞和遗传机制了解很少。在这里，我们表明，在细胞分裂和细胞扩增中的缺陷都在拟南芥木质素突变体ref8的矮化基础上，并报告了从抑制物筛选中鉴定出生长抑制释放1（GIR1）基因。GIR1编码MYB4的核导入所需的importin-beta-like蛋白，MYB4是苯丙烷代谢的转录阻遏物。GIR1的破坏和MYB4类似地减轻蜂窝缺陷和生长抑制在REF8，这表明生长援救效果gir1可能是由于受损MYB4运输和功能。重要的是，在gir1 ref8和myb4 ref8中苯丙类化合物的扰动并没有得到缓解，这表明MYB4在木质素修饰植物的生长抑制中的功能可能与已知的其在苯丙素类生物合成基因的转录调控中的作用不同。这项研究还提供了证据，证明木质素修饰引起的侏儒症不仅是由于木质素缺乏导致的水运输受到损害，例如gir1。 对表现出塌陷的木质部表型的其他木质素突变体的生长抑制没有影响。