Open AccessPolycomb group-dependent imprinting of the actin regulatorAtFH5regulates morphogenesis inArabidopsis thaliana
Author(s) -
Jonathan N. Fitz Gerald,
Poh Shi Hui,
Frédéric Berger
Publication year - 2009
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.036921
Subject(s) - biology , genomic imprinting , polycomb group proteins , homeotic gene , arabidopsis , genetics , gene silencing , agamous , histone , gene , microbiology and biotechnology , regulation of gene expression , transcription factor , regulator , transcription (linguistics) , gene expression , repressor , mutant , dna methylation , linguistics , philosophy
During embryogenesis, Polycomb group (PcG) complexes deposit silencing histone modifications and target homeotic genes, which regulate the patterning of other transcription factors. This transcriptional network further maintains cell fate. However, genome-wide identification of histone modifications has suggested that PcG complexes might regulate genes other than those encoding transcription factors. In Arabidopsis, we show that PcG activity directly targets the actin regulator formin ARABIDOPSIS FORMIN HOMOLOGUE 5 (AtFH5). PcG activity silences the paternal allele of AtFH5, restricting its expression to the maternal allele. AtFH5 thus appears to be a new, maternally expressed imprinted gene. We further demonstrate that AtFH5 is responsible for morphological defects caused by the loss of PcG activity in the seed.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom