Department of Biology, Pennsylvania State University, University Park, PA, USA.
Plant Signal Behav. 2010 Jun;5(6):687-90. doi: 10.4161/psb.5.6.11575. Epub 2010 Jun 1.
The functions of dicot sucrose transporters (SUTs) in apoplastic phloem loading of sucrose are well established; however, whether SUTs similarly function in monocots was unresolved. To address this question, we recently provided genetic evidence that ZmSUT1 from maize (Zea mays) is required for efficient phloem loading. sut1-m1 mutant plants hyperaccumulate carbohydrates in leaves, are defective in loading sucrose into the phloem, and have altered biomass partitioning. Presumably due to the hyperaccumulation of soluble sugars in leaves, mutations in ZmSUT1 lead to downregulation of chlorophyll accumulation, photosynthesis and stomatal conductance. However, because we had identified only a single mutant allele, we were not able to exclude the possibility that the mutant phenotypes were instead caused by a closely linked mutation. Based on a novel aspect of the sut1 mutant phenotype, secretion of a concentrated sugar solution from leaf hydathodes, we identified an additional mutant allele, sut1-m4. This confirms that the mutation of SUT1 is responsible for the impairment in phloem loading. In addition, the sut1-m4 mutant does not accumulate transcripts, supporting the findings reported previously that the original mutant allele is also a null mutation. Collectively, these data demonstrate that ZmSUT1 functions to phloem load sucrose in maize leaves.
双子叶植物蔗糖转运蛋白(SUTs)在质外体韧皮部中蔗糖装载的功能已得到充分证实;然而,SUTs 是否同样在单子叶植物中起作用仍未解决。为了解决这个问题,我们最近提供了遗传证据,表明玉米(Zea mays)中的ZmSUT1 是有效韧皮部装载所必需的。sut1-m1 突变体植物在叶片中过度积累碳水化合物,蔗糖装载到韧皮部的能力受损,生物量分配发生改变。由于叶片中可溶性糖的过度积累,ZmSUT1 的突变导致叶绿素积累、光合作用和气孔导度下降。然而,由于我们只鉴定出一个突变等位基因,因此不能排除突变表型是由紧密连锁的突变引起的可能性。基于 sut1 突变体表型的一个新方面,即叶片水孔从叶片中分泌浓缩糖溶液,我们鉴定出了另一个突变等位基因 sut1-m4。这证实了 SUT1 的突变是导致韧皮部装载受损的原因。此外,sut1-m4 突变体不积累转录本,这支持了之前报道的原始突变等位基因也是无效突变的发现。总的来说,这些数据表明 ZmSUT1 在玉米叶片中负责韧皮部装载蔗糖。