TY - JOUR
T1 - Kdx1 regulates RCK1 gene expression by interacting with Rlm1 in Saccharomyces cerevisiae
AU - Chang, Miwha
AU - Kang, Hyun Jun
AU - Baek, In Joon
AU - Kang, Chang Min
AU - Park, Yong Sung
AU - Yun, Cheol Won
N1 - Funding Information:
This work was supported by a National Research Foundation of Korea ( NRF ) grant funded by the Korean government ( MEST ) (No. 2011-0017050 ).
PY - 2013/6/7
Y1 - 2013/6/7
N2 - Kdx1 is known as a stress-responsive protein. To better understand the function of Kdx1, we performed microarray analysis in KDX1 overexpressing cells and found that the overexpression of KDX1 dramatically induced the expression of RCK1, a stress-responsive gene. This result was confirmed by northern blot analysis. Furthermore, the overexpression of RCK1 partially rescued the growth defect caused by zymolyase stress. The expression of RCK1 was regulated independently by Slt2 and Hog1, and Kdx1 failed to induce the expression of RCK1 in a HOG1 deletion strain. The transcriptional factors Smp1, Sko1, Msn2, Msn4, and Hot1, which are regulated by Hog1, did not affect RCK1 expression, but Rlm1 did. Furthermore, the mutation of certain phosphorylation sites in RLM1 inhibited the induction of RCK1 expression by Kdx1. We found a conserved Rlm1 binding site in the 5' untranslated region (UTR) of RCK1, and the mutation of these Rlm1 binding sites also inhibited the induction of RCK1 expression by Kdx1. Finally, we showed that Kdx1 physically interacts with Rlm1 and that this interaction affects the ability of Rlm1 to bind to the RCK1 5' UTR. Taken together, these data suggest that Kdx1 interacts with Rlm1 to activate RCK1 gene expression in response to stress in Saccharomyces cerevisiae.
AB - Kdx1 is known as a stress-responsive protein. To better understand the function of Kdx1, we performed microarray analysis in KDX1 overexpressing cells and found that the overexpression of KDX1 dramatically induced the expression of RCK1, a stress-responsive gene. This result was confirmed by northern blot analysis. Furthermore, the overexpression of RCK1 partially rescued the growth defect caused by zymolyase stress. The expression of RCK1 was regulated independently by Slt2 and Hog1, and Kdx1 failed to induce the expression of RCK1 in a HOG1 deletion strain. The transcriptional factors Smp1, Sko1, Msn2, Msn4, and Hot1, which are regulated by Hog1, did not affect RCK1 expression, but Rlm1 did. Furthermore, the mutation of certain phosphorylation sites in RLM1 inhibited the induction of RCK1 expression by Kdx1. We found a conserved Rlm1 binding site in the 5' untranslated region (UTR) of RCK1, and the mutation of these Rlm1 binding sites also inhibited the induction of RCK1 expression by Kdx1. Finally, we showed that Kdx1 physically interacts with Rlm1 and that this interaction affects the ability of Rlm1 to bind to the RCK1 5' UTR. Taken together, these data suggest that Kdx1 interacts with Rlm1 to activate RCK1 gene expression in response to stress in Saccharomyces cerevisiae.
KW - Cell wall stress
KW - Hog1
KW - Kdx1
KW - Rck1
KW - Saccharomyces cerevisiae
UR - http://www.scopus.com/inward/record.url?scp=84879003855&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2013.04.083
DO - 10.1016/j.bbrc.2013.04.083
M3 - Article
C2 - 23660188
AN - SCOPUS:84879003855
VL - 435
SP - 350
EP - 355
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -