|
|
|
|||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
First published online September 25, 2009
doi: 10.1242/10.1242/dev.036921
Research Report |

1 Temasek Life Sciences Laboratory, 1 Research Link, National University of
Singapore, Singapore 117604.
2 Department of Biological Sciences, National University of Singapore, 14
Science Drive, 4 Singapore 117543.
Author for correspondence
(fred{at}tll.org.sg)
Accepted 19 August 2009
SUMMARY
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.
Key words: Polycomb, Endosperm, Arabidopsis, Imprinting, ARABIDOPSIS FORMIN HOMOLOGUE 5 (AtFH5)
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati
Twitter What's this?