Low-temperature stress induces the expression of a variety of genes in
plants. However, the signal transduction pathway(s) that activates ge
ne expression under cold stress is poorly understood. Mutants defectiv
e in cold signaling should facilitate molecular analysis of plant resp
onses to low temperature and eventually lead to the identification and
cloning of a cold stress receptor(s) and intracellular signaling comp
onents. In this study, we characterize a plant mutant affected in its
response to low temperatures. The Arabidopsis hos1-1 mutation identifi
ed by luciferase imaging causes superinduction of cold-responsive gene
s, such as RD29A, COR47, COR15A, KIN1, and ADH. Although these genes a
re also induced by abscisic acid, high salt, or polyethylene glycol in
addition to cold, the hos1-1 mutation only enhances their expression
under cold stress. Genetic analysis revealed that hos1-1 is a single r
ecessive mutation in a nuclear gene. Our studies using the firefly luc
iferase reporter gene under the control of the cold-responsive RD29A p
romoter have indicated that cold-responsive genes can be induced by te
mperatures as high as 19 degrees C in hos1-1 plants. In contrast, wild
-type plants do not express the luciferase reporter at 10 degrees C or
higher. Compared with the wild type, hos1-1 plants are less cold hard
y, Nonetheless, after 2 days of cold acclimation, hos1-1 plants acquir
ed the same degree of freezing tolerance as did the wild type. The hos
1-1 plants flowered earlier than did the wild-type plants and appeared
constitutively vernalized, Taken together, our findings show that the
HOS1 locus is an important negative regulator of cold signal transduc
tion in plant cells and that it plays critical roles in controlling ge
ne expression under cold stress, freezing tolerance, and flowering tim
e.