Hipersensibilidade a dano do DNA em nichos de células-tronco de plantas

Hypersensitivity to DNA damage in plant stem cell niches

Nick Fulcher and Robert Sablowski1

- Author Affiliations

Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, United Kingdom

Edited by Elliot M. Meyerowitz, California Institute of Technology, Pasadena, CA, and approved October 14, 2009 (received for review August 13, 2009)

Abstract

The growing apices of plants contain stem cells that continually produce tissues, which, in the shoot, include the germline. These stem cell populations remain active throughout the plant's life, which can last for centuries, and are particularly exposed to environmental hazards that cause DNA damage and mutations. It is not known whether plants have mechanisms to safeguard the genome specifically in these crucial cell populations. Here, we show that root and shoot stem cells and their early descendants are selectively killed by mild treatment with radiomimetic drugs, x-rays, or mutations that disrupt DNA repair by nonhomologous end-joining. Stem cell death required transduction of DNA damage signals by the ATAXIA-TELANGIECTASIA MUTATED (ATM) kinase and, specifically in the root, also the ATM/RAD3-RELATED (ATR) kinase. Consistent with the absence of p53 and the core apoptotic machinery in plants, death of the stem cells did not show apoptotic but autolytic features as seen in other cases of plant developmentally programmed cell death. We propose that plants have independently evolved selective death as a stringent mechanism to safeguard genome integrity in their stem cell populations.

Arabidopsis double-strand breaks meristem programmed cell death

Footnotes

1To whom correspondence should be addressed. E-mail: robert.sablowski@bbsrc.ac.uk

Author contributions: N.F. and R.S. designed research; N.F. and R.S. performed research; N.F. and R.S. analyzed data; and R.S. wrote the paper.

The authors declare no conflict of interest.

This article is a PNAS Direct Submission.

This article contains supporting information online at www.pnas.org/cgi/content/full/0909218106/DCSupplemental.

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