Amino Acids

, Volume 40, Issue 2, pp 623–631 | Cite as

Mcm1p binding sites in the ARG1 promoter positively regulate ARG1 transcription and S. cerevisiae growth in the absence of arginine and Gcn4p

Original Article


In this study, we investigated the activating role of Mcm1p at ARG1 during arginine starvation. Our results showed that two Mcm1p binding sites positively contribute to ARG1 transcription and cell growth. Especially, we provide strong evidence that the Mcm1p binding sites play a positive role in ARG1 transcription to overcome arginine starvation in the absence of Gcn4p. In addition, we found that the Mcm1p binding sites are not only regulated by the presence or absence of arginine but also in the presence or absence of other amino acids. These findings suggest that the ARG1 promoter utilizes different DNA elements to control transcription, depending on which amino acids are detected in the medium.


Gcn4p Mcm1p ARG1 SD and SC media Arginine starvation 



Synthetic defined minimal


Synthetic defined complete


Arginine control


MCM1, AGAMOUS, DEFICIENS, and serum response factor


Wild type









We thank Marjolaine Crabeel for the SS5 strain and M13mp7-ARG1. This work was supported by Basic Science Program through the National Research Foundation of Korea Grant funded by the Korean Government (NRF-2009-0070791).

Supplementary material

726_2010_687_MOESM1_ESM.tif (942 kb)
Supplementary Figure 1. Two Mcm1p binding sites have suppressive function in GCN4 deletion strain for survival during arginine starvation. (A and B) The gcn4ΔSS5 strains containing mutated ARG1 alleles are indicated on the left. (See Table 1 for description of strains.) “No” indicates WT ARG1 promoter in gcn4Δ SS5 strains. Cells were grown to saturation in SD+URA medium at 30°C, serially diluted tenfold, and spotted onto SD+ARG, SD, SD+Can (Canavanine; 0.05 μg/ml), or SC-ARG supplemented with uracil. The growth phenotype following more than two days’incubation at 30°C is shown. (TIFF 941 kb)
726_2010_687_MOESM2_ESM.doc (42 kb)
Supplementary material 2 (DOC 41 kb)


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Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  1. 1.Research InstituteNational Cancer CenterGoyang-siRepublic of Korea
  2. 2.Lee Gil Ya Cancer and Diabetes InstituteGachon University of Medicine and ScienceIncheonRepublic of Korea

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