A contradictoryGLABRA3allele helps define gene interactions controlling trichome development inArabidopsis

Abstract

Previously characterized Arabidopsis gl3 mutants have trichomes that are smaller, less branched and undergo fewer rounds of endoreplication than wild-type trichomes. A new gl3 mutant, called gl3-sst, has oddly shaped trichomes that over expand during early development, undergo more endoreduplication and that have a striking nuclear morphology. The mutant nuclei consist of many interconnected lobes; however, only a single set of polytenelike chromosomes reside in the mutant nuclei. The predicted gl3-sst polypeptide has a Leu to Phe substitution (codon 78) within a region responsible for protein-protein interaction. 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.Furthermore, TRY has the ability to prevent the GL1 GL3 interaction and the GL1 gl3-sst interaction is even more sensitive to TRY. Analysis of plants expressing functional GFP-tagged versions of GL1, GL3 and TRY show that the proteins are localized in trichome nuclei. These results have been used to model trichome initiation in terms of protein interactions and threshold levels of activator complex.Supplemental data available online

Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning inArabidopsis

“…5F; see If the abnormal distribution of GL3 in urm9 disrupts the function of GL3, one might expect URM9 to show genetic interaction with GL3. A gain-of-function allele of GL3, gl3-sst, produces various distorted trichomes, resembling those produced by the strong overexpressor of GL3 (Esch et al, 2003). As expected, the urm9 gl3-sst double mutant largely suppressed the gl3-sst trichome phenotype (Fig.…”

“…It is possible that the expression of the latter class of GL1 targets is dependent on the transcriptional activator domain of GL3 (Payne et al, 2000) and we speculate that such genes might include cell cycle regulators that direct DNA endoreduplication, the first committed step of trichome initiation. This view is supported by the finding that the loss-and gain-offunction of GL3 specifically alter the endoreduplication cycle of trichomes (Hülskamp et al, 1994;Esch et al, 2003).…”

“…The following mutants and transgenic lines have been described previously: aos (Park et al, 2002); coi1-1 (Xie et al, 1998); egl3-7 (SALK_077439), gl1-20990 and gl3-sst (Esch et al, 2003); gl1-1 (Oppenheimer et al, 1991); gl1-2 (Esch et al, 1994); jar1-1 (Staswick et al, 2002); myb23-1 (Kirik et al, 2005); myc2-1 (Boter et al, 2004); sad2-2 (Verslues et al, 2006); GL1::GUS (Larkin et al, 1993); GL2::GUS (Szymanski et al, 1998); MYB23::GUS (Kirik et al, 2001); CPC::GFP ; VSP1::GUS (Ellis et al, 2001). aos and coi1-1 were backcrossed to wild type Col-0 because the original lines had gl1 markers and lacked trichomes.…”

Arabidopsis TRANSPARENT TESTA GLABRA2Is Directly Regulated by R2R3 MYB Transcription Factors and Is Involved in Regulation ofGLABRA2Transcription in Epidermal Differentiation

“…GLABROUS1 (GL1), which is functionally equivalent to WER, is thought to form a transcriptional complex with GL3/ EGL3 and TTG1 to promote GL2 expression in trichomes (Szymanski et al, 1998;Payne et al, 2000;Lee and Schiefelbein, 2001;Zhang et al, 2003). Mutations in GL1, GL3, EGL3, TTG1, and GL2 result in a reduction in trichome number and lessbranched trichomes, except for mutants with the gl3-sst allele (Koornneef et al, 1982;Esch et al, 2003;Zhang et al, 2003). CPC and its homolog, TRIPTYCHON (TRY), are transcribed in trichomes and affect trichome distribution (Schellmann et al, 2002).…”

“…These mutant phenotypes suggest that CPC and TRY suppress trichome initiation by lateral inhibition. It has been proposed that CPC and TRY translated in trichomes move to neighbor epidermal cells, where they prevent GL1-GL3/EGL3 interaction by competition with GL1 for GL3/EGL3 binding sites (Esch et al, 2003).…”