Members of the GCN5 Histone Acetyltransferase Complex Regulate PLETHORA-Mediated Root Stem Cell Niche Maintenance and Transit Amplifying Cell Proliferation inArabidopsis 

Abstract

The PLETHORA (PLT) stem cell transcription factors form a developmentally instructive protein gradient in Arabidopsis thaliana roots. Histone acetylation is known to facilitate gene transcription and plays an important role in developmental processes. Here, we show that histone acetyltransferase GCN5 (for general control nonderepressible 5) attenuates the PLT gradient. Based on genetic evidence, we establish that GCN5 is essential for root stem cell niche maintenance and acts in the PLT pathway. The GCN5-associated factor ADA2b (for alteration/deficiency in activation 2b) is also positioned in the PLT pathway and regulates PLT expression, similar to GCN5. Both GCN5 and ADA2b mediate proliferation of the transit amplifying cells, but ADA2b does not affect stem cell niche maintenance. Overexpression of PLT2 rescues the stem cell niche defect of gcn5 mutants, indicating that GCN5 regulation of PLT expression is essential for maintenance of the root stem cell niche. We conclude that histone acetylation complexes play an important role in shaping a developmentally instructive gradient in the root.

Impact of nucleosome dynamics and histone modifications on cell proliferation during Arabidopsis development

“…The pleiotropic effects of gcn5 mutation on plant growth and development suggest that it is required at various developmental stages, for example, the control of floral meristem development by regulating the expression of WUSCHEL (WUS) and AGAMOUS (AG) genes (Bertrand et al, 2003;Vlachonasios et al, 2003). GCN5 and its partner ADA2b regulate stem cell niche maintenance through the PLETHORA (PLT) pathway (Kornet and Scheres, 2009). Additionally, WUS expression in the floral meristem depends on KNUCKLES (KNU), a C2H2-type zinc finger repressor protein whose expression is inhibited by the presence of H3K27me3 marks in the SAM and is later activated by AG to terminate stem cell activity (Sun et al, 2009).…”

Putative Arabidopsis Transcriptional Adaptor Protein (PROPORZ1) is required to modulate histone acetylation in response to auxin

“…Auxin-inducible expression of PLT2, a potential target for Arabidopsis SAGA activity (12,17), no longer exhibited a comparable response to auxin in prz1-1 (Fig. S2).…”

“…For example, PLT1 and PLT2 (PLETHORA), two transcription factors that redundantly control stem cell niche establishment in root meristems (17), exhibit reduced expression in atgcn5 and prz1 (12). Overexpression of PLT2 partially rescues atgcn5 root meristem defects, suggesting that diminished PLT abundance interferes with proper meristem function in Arabidopsis SAGA complex mutants (12).…”

“…Mutations in PRZ1 and AtGCN5 cause pleiotropic alterations in pattern formation and organogenesis also manifested as defects in the interpretation of signals relevant for plant morphogenesis (7,8,(12)(13)(14). Furthermore, PRZ1 and AtGCN5 appear to be essential for adaptive growth, reflected in altered stress responsiveness of the corresponding mutant alleles (8,15) Consistent with these pleiotropic phenotypes, ChIP experiments demonstrated that AtGCN5 associates with about one third of approximately 20,000 Arabidopsis promoter regions analyzed (16), which correlates with misexpression of a substantial fraction of the Arabidopsis transcriptome in atgcn5 and prz1 alleles (8).…”

The Arabidopsis transcription factor bZIP11 activates auxin-mediated transcription by recruiting the histone acetylation machinery

“…Several data sets support the impact of histone acetylation on auxin signalling. In fact, gcn5 and ada2b mutants, in which SAGA complex formation should be disrupted, exhibit several abnormal auxin-related growth phenotypes 20,[22][23][24] . Moreover, GCN5 has been found in a mutant suppressor screen for the corepressor TPL 24 and ADA2b was shown to be required for histone acetylation in response to auxin 25 .…”