The bHLH protein MUTE, stomata and the hydathode pore

Photo credit: Oxford Academic

Ectopic overexpression of MUTE over-rides organ- and cell file-specific rules. (A, B) DIC image of wild type (A) and 35S::MUTE (B) petal epidermis. The asterisk indicates aberrant shaped stomata. (C–J) Hypocotyl epidermis of WT (C), ttg(D), gl2 (E), ttg; mute (F), gl2; mute (G), er; erl1; erl2 (H), tmm (I), 35S::MUTE (J). Arrowheads indicate protruding cell files with ectopic stomata or meristemoids. Scale bar, 20 μm.

The bHLH protein, MUTE, controls differentiation of stomata and the hydathode pore in Arabidopsis.

by Pillitteri L. J., Bogenschutz N. L., Torii K. U. (2008)

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Lynn Jo Pillitteri, Western Washington University, Bellingham, WA, USA
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Naomi L. Bogenschutz, University of Washington, USA
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Keiko U. Torii, University of Washington, USA

in Plant Cell Physiol 49:934–943. – DOI:https://doi.org/10.1093/pcp/pcn067 – 

Abstract/FREE Full TextGoogle Scholar – 

https://academic.oup.com/pcp/article/49/6/934/1811933/The-bHLH-Protein-MUTE-Controls-Differentiation-of?ijkey=a82b0b2306ff4bfe69c873557ad45343c29fd352&keytype2=tf_ipsecsha

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Proposed model for inhibitory regulation of stomatal differentiation. (A) The signal transduction cascade through YODA, the ER-family and TMM inhibits the action of a meristemoid-specific factor ‘X’, which requires MUTE to direct stomatal differentiation. In mute (B), the signal transduction cascade exerts inhibition on factor ‘X’ and, with no MUTE protein present, stomatal differentiation does not take place. Under conditions of reduced inhibitory signaling and MUTE loss of function (C), the inhibition on factor ‘X’ is lifted and, even in the absence of MUTE, can restore a minimal amount of stomatal differentiation. – https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/pcp/49/6/10.1093/pcp/pcn067/2/m_pcn067f7.gif?Expires=1487293493&Signature=IsV2RuM3B3PfWk74STmrXt8ACvyxAmg-xlc~D0jgY8uliVP5SjAmOHtrCvBsupWoE7P8WSCDWOKfbu9ue8gva7EjfPLMz50FbGS-c6vrTYaEESAyIWfLyHYivVqfzzlqgquwNOzvsHVgD8vaYeadYJ2UwgqxBjJ5nFn~xXYaK07paI9pwWDdVbZpWlmwNygc-ooPmZXl3zR3ldAr7T-coztf5l5LQJ7eGeeBBmTRp0rCaUn3MlGPwvoDwzxwY6yVEo1nWiduXxtlhnicTB3upytYlBOGjht9uAj9Pr-ynDoAhIJzG8D6IsgQ~ZvDPqOxYrdpnpgHtIZDqGexz8VJkg__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q

Abstract

Stomata are turgor-driven epidermal valves on the surface of plants that allow for efficient gas and water exchange between the plant and its environment.The Arabidopsis thaliana basic helix–loop–helix (bHLH) protein, MUTE, is a master regulator of stomatal differentiation where it is required for progression through the stomatal lineage and the differentiation of stomata.

The genetic control of stomatal spacing across the epidermal surface is variable in different organs. For instance, a distinct suite of genes from those in leaves regulates stomatal patterning in hypocotyls.

Here we report that regardless of organ type, MUTE controls downstream events directing stomatal differentiation, specifically the transition from meristemoid to guard mother cell.

Ectopic MUTE expression is sufficient to over-ride cell fate specification in cell types that do not normally differentiate stomata. Furthermore, MUTE is required for the production of the structure evolutionarily related to stomata, the hydathode pore.

Consistently, MUTE displays expression at the tip of cotyledons and leaves, thus co-localizing with the auxin maxima. However, MUTE itself was not regulated by the auxin, and the absence of hydathode pores in mute did not affect the auxin maxima.

Surprisingly, our analysis revealed that the requirement for MUTE could be partially circumvented under conditions of compromised inhibitory signaling.

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Published by

Willem Van Cotthem

Honorary Professor of Botany, University of Ghent (Belgium). Scientific Consultant for Desertification and Sustainable Development.

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