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