Hd1 repressor function can be enhanced by casein kinase
2 (CK2) activity that includes Hd6 protein as the CK2a
subunit. Hd6 CK2awas first identified as a QTL that
delays flowering, and interestingly, this effect appears in a
LD-specific manner [36]. Extensive molecular genetic
studies revealed that Hd6 CK2aclearly delays flowering
and efficiently suppresses Hd3aexpression only when
Hd1is functional. However, Hd6 CK2adoes not phosphorylate Hd1 protein directly, suggesting the presence
of an unknown substrate that is expected to work with
Hd1 [37].
Hd3a expression is upregulated by not only Hd1 but also
Ehd1, and the latter is suppressed by Ghd7, which is a
small protein with a CCT-domain [13
]. Ghd7is also
unique to rice with no counterpart in Arabidopsis. Another
key mechanism for photoperiodicHd3aexpression comes
[19
]. In se5, Hd1 protein always acts as the activator of
Hd3a independent of day length, suggesting that phytochrome signaling converts Hd1 into a repressor.
This finding is further supported by the direct manipulation ofOsGIexpression and the resulting change in
Hd1andHd3aexpression levels [12
]. Hd1expression
peaks at midnight under SD. Thus, Hd1 protein normally
does not accumulate at a time when phytochrome signaling occurs. However, whenOsGIis overexpressed,Hd1
expression gets higher in the daytime, allowing Hd1
protein to interact with the phytochrome signaling pathway, resulting in the conversion of Hd1 to a repressor of
Hd3aexpression.