The metabolism of C1 compounds in higher plants is an attractive research target. Plant growth test under various C1 compounds showed that formate stimulates the growth of young rice plant. The feeding experiment with ^<13>C-HCOOH and ^<13>C-CH_3OH revealed that these two compounds were readily incorporated from the root and converted into CO_2 by the stepwise oxidation pathway. Application of formate to the root part of the rice plant induced the increase of the activity of formate dehydrogenase (FDH) responsible for the conversion reaction of formate into CO_2 and also the accumulation of mRNA of FDH in the root part. These results indicated that formate could enhance plant growth under the CO_2-limited condition. Strong sunlight is known to be harmful to photosynthesis under CO_2-depleted conditions. This phenomenon is understood as photoinhibition. Application of potassium formate or methanol before the photoinhibitory treatment could lower the damage of rice photosynthesis from photoinhibition. This fact indicated that the substantial concentration of antioxidants capable of protecting PS II from photooxidative damage is not always endorsed and it is strongly suggested that formate is involved in endogenous radical scavenging mechanisms or formate (and/or its metabolite) suppresses ROS generation in the vicinity of the damage site of PS II. The other non-natural C1 compounds are also tested using rice as an experimental plant. Rice plant growth test revealed that methylamine treatment inhibited the aerial part but stimulated the growth of root part. The gene homologue of cytosolic phosphoglycerate kinase was isolated as the gene, which was stimulated by methylamine treatment, by differential display RT-PCR method. Further Northern blot analysis of the genes related to glycolytic pathway indicated that glycolysis stimulated by methyl amine treatment. A series of result mentioned above indicates that exogenous C1 compounds should be activated specific genes. That is interesting as a result suggesting the existence of specific signal-transducing pathway for exogenous C1 compounds.