Plants have evolved a network of complex signaling pathways that allow them to cope with the fluctuations of internal and external environmental cues. GIGANTEA (GI), a well-known, highly conserved plant nuclear protein, has been shown to regulate multiple biological functions in plants such as circadian rhythm, light signaling, cold tolerance, hormone signaling, and photoperiodic flowering. Recently, the role of GI in disease tolerance against different pathogens has come to light; however, a detailed mechanism to understand the role of GI in pathogen defense remains largely unexplained. Here, we report that
GIGANTEA
is upregulated upon infection with a virulent oomycete pathogen,
Hyaloperonospora arabidopsidis
(
Hpa
), in
Arabidopsis thaliana
accession Col-0. To investigate the role of GI in
Arabidopsis
defense, we examined the pathogen infection phenotype of
gi
mutant plants and found that
gi-100
mutant was highly susceptible to
Hpa
Noco2 infection. Notably, the quantitative real-time PCR showed that
PHYTOALEXIN DEFICIENT4
(
PAD4
) and several PAD4-regulated downstream genes were downregulated upon Noco2 infection in
gi-100
mutant as compared to Col-0 plants. Furthermore, the chromatin immunoprecipitation results show that GI can directly bind to the intronic region of the
PAD4
gene, which might explain the mechanism of GI function in regulating disease resistance in plants. Taken together, our results suggest that
GI
expression is induced upon
Hpa
pathogen infection and GI can regulate the expression of
PAD4
to promote resistance against the oomycete pathogen
Hyaloperonospora arabidopsidis
in
Arabidopsis thaliana
.