Land plants have evolved a cuticle-bearing epidermis to protect themselves from environmental stress and pathogen attack. Despite its important role, little is known about the molecular mechanisms regulating shoot epidermal cell identity. In a recent study, we found that the Arabidopsis thaliana ATML1 gene is possibly a master regulator of shoot epidermal cell fate. We revealed that ATML1 has the ability to confer shoot epidermis-related traits to non-epidermal cells of the seedlings. These data are consistent with the previous loss-of-function mutant analyses, which implied a positive role of ATML1 in epidermal cell differentiation. Importantly, ectopic epidermal cells induced in ATML1-overexpressing lines provide a novel tool to assess the intrinsic properties of epidermal cells and to study epistatic interactions among genes involved in epidermal/mesophyll differentiation. Using this system, we obtained data revealing that ATML1 negatively influenced mesophyll cell fate. In addition, we provided a working model of how division planes in epidermal cells are determined.The specification of plant shoot epidermal cells during development remains unknown. It has been suggested that ATML1, an HD-ZIP class IV transcription factor, is a key regulator of epidermal cell differentiation.1 ATML1 is specifically expressed in the shoot epidermis, and loss-of-function mutations in ATML1 and its closest homolog PDF2 severely affect epidermal cell differentiation of leaves. [1][2][3][4] We recently reported ATML1 gain-of-function experiments for the first time, and revealed that ATML1 is able to confer epidermal cell fate in non-epidermal tissues of the seedlings. 5 In this addendum, we summarize and further discuss our major findings and provide a perspective for future research in this field.
ATML1 Activates the Expression of Epidermis-Specific GenesOur overexpression studies revealed that ATML1 activated expression of several epidermis-specific genes, which contain ATML1-binding sites (L1 box) in their promoters, suggesting that ATML1 acts on the promoters of these genes.
5,6However, not all the L1 box-containing genes tested were upregulated in ATML1-overexpressing lines.5 For example, PDF1 was not significantly upregulated in ATML1-overexpressing plants, whereas loss of ATML1 and PDF2 activity resulted in decreased PDF1 expression.