HISTONE DEACETYLASE 19 and the flowering time gene FD maintain reproductive meristem identity in an age-dependent manner

Mutation of the chromatin regulator HDA19 causes age-dependent patterning defects in reproductive meristems. This effect is enhanced by mutation of FD, revealing a novel developmental role for this flowering time gene. Abstract The shoot apical meristem (SAM) undergoes developmental transitions that...

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Veröffentlicht in:Journal of experimental botany 2018-09, Vol.69 (20), p.4757-4771
Hauptverfasser: Gorham, Sasha R, Weiner, Aaron I, Yamadi, Maryam, Krogan, Naden T
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Sprache:eng
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Zusammenfassung:Mutation of the chromatin regulator HDA19 causes age-dependent patterning defects in reproductive meristems. This effect is enhanced by mutation of FD, revealing a novel developmental role for this flowering time gene. Abstract The shoot apical meristem (SAM) undergoes developmental transitions that include a shift from vegetative to reproductive growth. This transition is triggered by flowering time genes, which up-regulate floral meristem (FM) identity genes that, in turn, control flower development by activating floral organ identity genes. This cascade of transcriptional activation is refined by repression mechanisms that temporally and spatially restrict gene expression to ensure proper development. Here, we demonstrate that HISTONE DEACETYLASE 19 (HDA19) maintains the identity of the reproductive SAM, or inflorescence meristem (IM), late in Arabidopsis thaliana development. At late stages of growth, hda19 IMs display a striking patterning defect characterized by ectopic expression of floral organ identity genes and the replacement of flowers with individual stamenoid organs. We further show that the flowering time gene FD has a specific function in this regulatory process, as fd hastens the emergence of these patterning defects in hda19 growth. Our work therefore identifies a new role for FD in reproductive patterning, as FD regulates IM function together with HDA19 in an age-dependent fashion. To effect these abnormalities, hda19 and fd may accentuate the weakening of transcriptional repression that occurs naturally with reproductive meristem proliferation.
ISSN:0022-0957
1460-2431
1460-2431
DOI:10.1093/jxb/ery239