On the cover: A shingleback lizard (Tiliqua rugosa) in defensive display shows off its characteristic bright blue tongue. In this issue, Brennan et al. explore how novel phenotypes—like the shingleback—arise through discontinuous evolutionary processes. In Australia, heterogeneous morphological evolution has led to an array of forms, from giant blue-tongue lizards to armored dwarf skinks. Photograph © Jules Farquhar; used with permission.
新植物学家：澳洲科学家揭示T6P与SL信号转导之间的关系
strigolactone (SL)抑制植物分支的形成，而 trehalose 6-phosphate (Tre6P) 则促进分支形成。作者发现在SL mutants 中差异表达的基因与Tre6P密切相关。于此同时Tre6P相关基因在豌豆的SL突变体中表达也发生了变化。 研究显示，Tre6P的水平在 SL signalling mutant more axillary (max) growth 2中的水平显著增高。 转基因研究显示提高Tre6P水平可以促进 levels demonstrated SL mutant 和 brc1提前开花。 Tre6P可以促进野生型分支数增多，但是对max2 and max4 mutants无用, 说明 Tre6P对分支数的调控依赖SL. Tre6P 可以提高brc1 mutants 的分支数，说明这两个途径之间可能 Tre6P在BRC2下游发挥作用。
小结：本研究揭示了Tre6P提高植物分支数的机制。
Schematic representation of the relationship between strigolactones, sucrose and Tre6P signalling. Tre6P is shown as being downstream of strigolactone signalling via a SUPPRESSOR OF MAX2-LIKE (SMXL)-dependent and independent pathway involving the inhibition of TRE6P SYNTHASE1 (TPS1) and TPS9. Tre6P acts in parallel to the know strigolactone signalling pathways involving BRC1. Tre6P also influences MAX2-dependent signalling by activating the flux into citrate which would lead to the inhibition of MAX2 on a protein level. This acts in parallel to the inhibition of MAX2 transcription by sucrose. Inhibition and activation are presented by blunt-ended blue or pointed red arrows, respectively. Currently, unknown interaction or interactions based on in vitro data are represented by dashed arrows. Black arrows represent processes. BRC1, BRANCHED1; CeTPP, Tre6P phosphatase from Caenorhabditis elegans; max, more axillary growth; otsA, Tre6P synthase from Escherichia coli; pGLDPA, GLYCINE-DECARBOXYLASE P-SUBUNIT A promoter from Flaveria trinervia; SMXL, SUPPRESSOR OF MAX2-LIKE.
原文：Strigolactone signalling inhibits trehalose 6-phosphate signalling independently of BRC1 to suppress shoot branching
