Genetic Control of Developmental Changes Induced by Disruption of Arabidopsis Histone Deacetylase 1 (AtHD1) Expression

Author:

Tian Lu12,Wang Jianlin1,Fong M Paulus13,Chen Meng1,Cao Hongbin4,Gelvin Stanton B4,Chen Z Jeffrey123

Affiliation:

1. Department of Soil and Crop Sciences and Intercollegiate Programs, Texas A&M University, College Station, Texas 77843-2474

2. Genetics, Texas A&M University, College Station, Texas 77843-2474

3. Molecular and Environmental Plant Sciences, Texas A&M University, College Station, Texas 77843-2474

4. Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392

Abstract

Abstract Little is known about the role of genetic and epigenetic control in the spatial and temporal regulation of plant development. Overexpressing antisense Arabidopsis thaliana HD1 (AtHD1) encoding a putative major histone deacetylase induces pleiotropic effects on plant growth and development. It is unclear whether the developmental abnormalities are caused by a defective AtHD1 or related homologs and are heritable in selfing progeny. We isolated a stable antisense AtHD1 (CASH) transgenic line and a T-DNA insertion line in exon 2 of AtHD1, resulting in a null allele (athd1-t1). Both athd1-t1 and CASH lines display increased levels of histone acetylation and similar developmental abnormalities, which are heritable in the presence of antisense AtHD1 or in the progeny of homozygous (athd1-t1/athd1-t1) plants. Furthermore, when the athd1-t1/athd1-t1 plants are crossed to wild-type plants, the pleiotropic developmental abnormalities are immediately restored in the F1 hybrids, which correlates with AtHD1 expression and reduction of histone H4 Lys12 acetylation. Unlike the situation with the stable code of DNA and histone methylation, developmental changes induced by histone deacetylase defects are immediately reversible, probably through the restoration of a reversible histone acetylation code needed for the normal control of gene regulation and development.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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