Abstract
Arabidopsis LEAFY COTYLEDON1 (LEC1) transcription factor is a master regulator that shapes plant embryo development and post-embryonic seedling establishment. Loss-of-function of LEC1 alters the cotyledon identity, causing the formation of ectopic trichomes, which does not occur in wild-type seedlings, implying that LEC1 might regulate embryonic cell fate determination during post-embryonic development. To test this hypothesis, we compared the expression of trichome development-related genes between the wild-type and the lec1 mutant. We observed that transcripts of GLABROUS1 (GL1), GL2, and GL3, genes encoding the positive regulators in trichome development, were significantly upregulated, while the TRICHOMELESS1 (TCL2), ENHANCER OF TRY AND CPC1 (ETC1), and ETC2 genes, encoding the negative regulators in trichome development, were downregulated in the lec1 mutant. Furthermore, overexpression of LEC1 activated the expressions of TCL2, CAPPICE (CPC), and ETC1, resulting in production of cotyledonary leaves with no or fewer trichomes during vegetative development. In addition, we demonstrated that LEC1 interacts with TCL2 in yeast and in vitro. A genetic experiment showed that loss-of-function of GL2 rescued the ectopic trichome formation in the lec1 mutant. These findings strongly support that LEC1 regulates trichome development, providing direct evidence for the role of LEC1 in cell fate determination during post-embryonic development.
Highlights
In higher plants, embryogenesis generally terminates with a dormancy period for future sporophyte growth
Among the trichome-positive genes, the expressions of GL1, GL2, and GL3 were significantly upregulated in the lec1 mutant compared with the wild-type, while those of ENHANCER OF GLABRA3 (EGL3) and TESTA GLABRA1 (TTG1) showed no change (Figure 2A)
The expressions of the trichome-negative genes TCL2, ENHANCER OF TRY AND CPC1 (ETC1), and ETC2 were significantly downregulated in the lec1 mutant compared with the wild-type, while those of TRY and CPC showed little change
Summary
Embryogenesis generally terminates with a dormancy period for future sporophyte growth. Ectopic expression LEC1 allows seedlings to remain in the embryonic state with an unexpanded cotyledon after germination and is sufficient to induce conversion of true leaves into embryonic structures that lack trichomes (Lotan et al, 1998; Junker et al, 2012) These findings support the multifunctional roles of LEC1 in embryonic and post-embryonic development. A small single-repeat R3 MYB protein family, including TRICHOMELESS1 (TCL1), TCL2, TRIPTYCHON (TRY), CAPPICE (CPC), ENHANCER OF TRY AND CPC1 (ETC1), and ETC2, plays redundant roles in the negative regulation of trichome development These proteins compete with GL1 for binding to GL3/EGL3, resulting in the formation of an inactive protein complex that fails to activate GL2 expression and represses trichome formation (Wang and Chen, 2014; Zhou et al, 2014)
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