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Proposed genetic pathway for the regulation of mucilage production during seed coat secretory cell differentiation. AP2 and
a TTG1 complex with a bHLH protein (candidates include EGL3 and/or TT8) and a tissue-specific MYB transcription factor activate
GL2 and TTG2. GL2 acts upstream of MUM4. In contrast, both TTG2 and MYB61 appear to affect aspects of mucilage production independent from MUM4. For details, see text.
Correct regulation of MUM4 transcription at the time of mucilage production does not require TTG2 or MYB61 (Fig. 7A). However, TTG1 is required to activate TTG2 in the seed coat (Fig. 7C) and in other tissues (Johnson et al., 2002). This result places TTG2 downstream from TTG1 in a second pathway that controls mucilage biosynthesis in the developing seed. This alternate pathway, along with another
that involves MYB61, may regulate the expression of other proteins involved in RGI synthesis including an NDP-d-GlcUA 4-epimerase (Feingold, 1982; Reiter and Vanzin, 2001), a nucleotide sugar transporter or an RGI-backbone glycosyltransferase. Alternatively, MYB61 and TTG2 may be involved in the transport of newly synthesized RGI to the plasma membrane. Feedback inhibition of mucilage production
in the absence of secretion has been demonstrated in the root caps of the maize (Zea mays) mutant Ageotropic (Millar and Moore, 1990).
AP2 encodes a putative transcription factor that is required for the differentiation of the outer two layers of the seed coat
(Western et al., 2001). Not surprisingly, ap2 seeds lack mucilage and fail to activate MUM4 transcription beyond its baseline level of expression (Fig. 7A). Although AP2 is required for maximum GL2 and TTG2 transcript levels (Fig. 7B), transcription of TTG1 and MYB61 was independent of AP2 activity (Fig. 7B). Our data are consistent with the hypothesis that AP2 functions in parallel with TTG1 to activate GL2 and TTG2 in the seed coat epidermis (Fig. 8).
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