College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, China.
BMC Plant Biol. 2011 Dec 15;11:176. doi: 10.1186/1471-2229-11-176.
Single-repeat R3 MYB transcription factors (single-repeat MYBs) play important roles in controlling trichome patterning in Arabidopsis. It was proposed that single-repeat MYBs negatively regulate trichome formation by competing with GLABRA1 (GL1) for binding GLABRA3/ENHANCER OF GLABRA3 (GL3/EGL3), thus inhibiting the formation of activator complex TTG1(TRANSPARENT TESTA GLABRA1)-GL3/EGL3-GL1 that is required for the activation of GLABRA2 (GL2), whose product is a positive regulator of trichome formation. Previously we identified a novel single-repeat MYB transcription factor, TRICHOMELESS1 (TCL1), which negatively regulates trichome formation on the inflorescence stems and pedicels by directly suppressing the expression of GL1.
We analyzed here the role of TRICHOMELESS2 (TCL2), a previously-uncharacterized single-repeat MYB transcription factor in trichome patterning in Arabidopsis. We showed that TCL2 is closely related to TCL1, and like TCL1 and other single-repeat MYBs, TCL2 interacts with GL3. Overexpression of TCL2 conferred glabrous phenotype while knockdown of TCL2 via RNAi induced ectopic trichome formation on the inflorescence stems and pedicels, a phenotype that was previously observed in tcl1 mutants. These results suggested that TCL2 may have overlapping function with TCL1 in controlling trichome formation on inflorescences. On the other hand, although the transcription of TCL2, like TCL1, is not controlled by the activator complex formed by GL1 and GL3, and TCL2 and TCL1 proteins are more than 80% identical at the amino acid level, the expression of TCL2 under the control of TCL1 promoter only partially recovered the mutant phenotype of tcl1, implying that TCL2 and TCL1 are not fully functional equivalent.
TCL2 function redundantly with TCL1 in controlling trichome formation on inflorescences, but they are not fully functional equivalent. Transcription of TCL2 is not controlled by activator complex formed by GL1 and GL3, but MIR156 controlled SQUAMOSA PROMOTER BINDING PROTEIN LIKE (SPL) transcription factors. However, SPLs might require co-activators to regulate the expression of their target genes, including TCL1, TRY and possibly, TCL2.
单重复 R3 MYB 转录因子（单重复 MYB）在控制拟南芥毛状体模式方面发挥重要作用。据推测，单重复 MYB 通过与 GLABRA1(GL1)竞争结合 GLABRA3/ENHANCER OF GLABRA3(GL3/EGL3)，从而负调控毛状体的形成，从而抑制 TTG1(TRANSPARENT TESTA GLABRA1)-GL3/EGL3-GL1 激活复合物的形成，该复合物对于 GLABRA2(GL2)的激活是必需的，GL2 的产物是毛状体形成的正调控因子。此前，我们鉴定了一个新的单重复 MYB 转录因子 TRICHOMELESS1(TCL1)，它通过直接抑制 GL1 的表达，负调控花序茎和花梗上的毛状体形成。
在这里，我们分析了先前未被表征的单重复 MYB 转录因子 TRICHOMELESS2(TCL2)在拟南芥毛状体模式形成中的作用。我们表明，TCL2 与 TCL1 密切相关，与 TCL1 和其他单重复 MYB 一样，TCL2 与 GL3 相互作用。TCL2 的过表达赋予了无毛表型，而通过 RNAi 敲低 TCL2 则在花序茎和花梗上诱导了异位毛状体的形成，这一表型以前在 tcl1 突变体中观察到。这些结果表明，TCL2 可能在控制花序毛状体形成方面与 TCL1 具有重叠功能。另一方面，尽管 TCL2 的转录不受由 GL1 和 GL3 形成的激活复合物的控制，并且 TCL2 和 TCL1 蛋白在氨基酸水平上有超过 80%的同一性，但在 TCL1 启动子控制下表达的 TCL2 仅部分恢复了 tcl1 的突变表型，这意味着 TCL2 和 TCL1 不是完全功能等效的。
TCL2 在控制花序毛状体形成方面与 TCL1 功能冗余，但它们不是完全功能等效的。TCL2 的转录不受由 GL1 和 GL3 形成的激活复合物的控制，而是受 MIR156 控制的 SQUAMOSA PROMOTER BINDING PROTEIN LIKE(SPL)转录因子控制。然而，SPL 可能需要共激活因子来调节其靶基因的表达，包括 TCL1、TRY，可能还有 TCL2。
