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Gene Review

GL3  -  transcription factor GLABRA 3

Arabidopsis thaliana

Synonyms: GLABRA 3, GLABROUS 3, MYC6.2
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High impact information on GL3

  • A network of putative transcriptional regulators, including the related bHLH proteins GLABRA3 (GL3) and ENHANCER OF GLABRA3 (EGL3), is known to influence the patterning of these cell types [1].
  • Further, the analysis of a GL3-YFP translational fusion, expressed under the GL3 promoter, indicates that the GL3 protein moves from the hair cells to the non-hair cells [1].
  • GLABRA3 (GL3) encodes a bHLH protein that interacts with the WD repeat protein, TTG1 [2].
  • Yeast interaction assays comparing GL3 with gl3-sst proteins show that the mutant protein interaction with GL1 and TTG1 is decreased by 75% and 50%, respectively, but there is no difference in its interaction with TRY [3].
  • The complex phenotype caused by ttg1 mutations is suppressed by ectopic expression of the maize anthocyanin regulator R. Here it is demonstrated that the Arabidopsis trichome development locus GLABRA3 (GL3) encodes an R homolog [4].

Biological context of GL3

  • Two Arabidopsis bHLH genes, GLABRA3 (GL3) and MYC-146, encode proteins that are similar throughout the predicted amino acid sequence to R and DELILA, which regulate anthocyanin production in maize and snapdragon, respectively [5].
  • Although they are thought to act in both the hair and non-hair cell types, we surprisingly found that GL3 and EGL3 gene expression and RNA accumulation occurs preferentially in the developing hair cells [1].

Other interactions of GL3

  • GL3 and GLABRA1 (GL1) interact when overexpressed together in plants [4].
  • However, transient expression of GL3 and MYC-146 upon microprojectile bombardment of petals of a white-flowered mutant of Matthiola incana was able to complement anthocyanin deficiency [5].
  • These findings, together with the results from our yeast two-hybrid analysis, suggest that GL3 gene function and overexpression of AtmybL2 act synergistically to inhibit trichome formation by negatively regulating GL2 expression [6].


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