1 ences matching binding sites for JUN/FOS and GRH transcription factors, but vary widely in trans- and

2                                           Ce-GRH-1 binds DNA in a sequence-specific manner identical

3                              In addition, Ce-GRH-1 binds to sequences upstream of the C.elegans gene

4                     The C.elegans member, Ce-GRH-1, groups with the Grainyhead subfamily, while the X

5                                 Grainy head (GRH) is a key transcription factor responsible for epide

6                 However, it is not known how GRH function is reactivated to repair differentiated epi

7                                     However, GRH with mutant ERK phosphorylation sites can still prom

8        Serine 91 is the principal residue in GRH that is phosphorylated by ERK.

9 r its DNA binding function, the ERK sites in GRH are required to activate Dopa decarboxylase (Ddc) an

10 utations of the ERK phosphorylation sites in GRH do not impair its DNA binding function, the ERK site

11 ur phylogenetic analysis of the expanded LSF/GRH family (including other previously unrecognized prot

12           We propose that the combination of GRH and FOS is part of an ancient wound-response pathway

13 s required for wound-dependent expression of GRH target genes in epidermal cells.

14                           Here, we show that GRH is directly regulated by extracellular signal-regula

15 sting that ERK sites are dispensable for the GRH function in establishing epidermal barrier integrity