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Journal of Experimental Botany 2008 59(12):3453-3464; doi:10.1093/jxb/ern195
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© 2008 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. This paper is available online free of all access charges (see
http://jxb.oxfordjournals.org/open_access.html for further details)


RESEARCH PAPER

Manganese deficiency alters the patterning and development of root hairs in Arabidopsis

Thomas Ju Wei Yang, Paula Jay Perry, Silvano Ciani, Sundaravel Pandian and Wolfgang Schmidt*

Institute of Plant and Microbial Biology, Academia Sinica, 115 Taipei, Taiwan

* To whom correspondence should be addressed. E-mail: wosh{at}gate.academia.sinica.edu.tw

Manganese (Mn) is the second most prevalent transition metal in the Earth's crust but its availability is often limited due to rapid oxidation and low mobility of the oxidized forms. Acclimation to low Mn availability was studied in Arabidopsis seedlings subjected to Mn deficiency. As reported here, Mn deficiency caused a thorough change in the arrangement and characteristics of the root epidermal cells. A proportion of the extra hairs formed upon Mn deficiency were located in atrichoblast positions, indicative of a post-embryonic reprogramming of the cell fate acquired during embryogenesis. When plants were grown under a light intensity of >50 µmol m–2 s–1 in the presence of manganese root hair elongation was substantially inhibited, whereas Mn-deficient seedlings displayed stimulated root hair development. GeneChip analysis revealed several candidate genes with potential roles in the reprogramming of rhizodermal cells. None of the genes that function in epidermal cell fate specification were affected by Mn deficiency, indicating that the patterning mechanism which controls the differentiation of rhizodermal cells during embryogenesis have been bypassed under Mn-deficient conditions. This assumption is supported by the partial rescue of the hairless cpc mutant by Mn deficiency. Inductively coupled plasma-optical emission spectroscopy (ICP-OES) analysis revealed that, besides the anticipated reduction in Mn concentration, Mn deficiency caused an increase in iron concentration. This increase was associated with a decreased transcript level of the iron transporter IRT1, indicative of a more efficient transport of iron in the absence of Mn.

Key words: Ion homeostasis, iron, light regulation, manganese, root hairs, transcriptional profiling

Received 22 May 2008; Revised 30 June 2008 Accepted 1 July 2008


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