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J Exp Bot. 2016 Aug;67(15):4779-89. doi: 10.1093/jxb/erw257. Epub 2016 Jul 6.

Protein N-terminal acetylation is required for embryogenesis in Arabidopsis.

Author information

1
College of Life Sciences, Capital Normal University, and Key Laboratory of Plant Gene Resources and Biotechnology for Carbon Reduction and Environmental Improvement, Beijing Municipal Government; Beijing 100048, China.
2
College of Life Sciences, Capital Normal University, and Key Laboratory of Plant Gene Resources and Biotechnology for Carbon Reduction and Environmental Improvement, Beijing Municipal Government; Beijing 100048, China ligeng.ma@cnu.edu.cn.

Abstract

Early embryonic development generates precursors of all major cell types in Arabidopsis. Among these precursors, the hypophysis divides asymmetrically to form the progenitors of the quiescent center and columella stem cells. A great deal has been learnt about the mechanisms that control the asymmetric division of the hypophysis and embryogenesis at the transcriptional level; however, no evidence of regulation at the co- or post-translational level has been reported. Here, we show that mutation of the catalytic subunit (Naa10) or auxiliary subunit (Naa15) of NatA, an N-terminal acetyltransferase that catalyzes protein N-terminal acetylation, produces an embryo-lethal phenotype. In addition, Naa10 and Naa15 were found to interact physically in planta Further analysis revealed that the observed embryonic patterning defects started at the early globular stage and that the asymmetric division of the hypophysis was irregular; thus, no quiescent center progenitor cells were generated in naa10 and naa15 embryos. We further observed that the polar distributions of auxin and its efflux carrier PIN1 were disturbed in naa10 embryos. Our results suggest that NatA is required for asymmetric division of the hypophysis and early embryonic patterning in Arabidopsis, and provides a link between protein N-terminal acetylation and embryogenesis in plants.

KEYWORDS:

Arabidopsis; NatA; asymmetric division; embryogenesis; hypophysis; protein N-terminal acetylation.

PMID:
27385766
PMCID:
PMC4973746
DOI:
10.1093/jxb/erw257
[Indexed for MEDLINE]
Free PMC Article

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