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Gene Review

CAD1  -  protein constitutively activated cell death 1

Arabidopsis thaliana

Synonyms: F15D2.24, F15D2_24, constitutively activated cell death 1
 
 
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Disease relevance of CAD1

  • Extracts of Escherichia coli cells expressing a CAD1 cDNA or the S. pombe gene catalyzing GSH-dependent, heavy metal-activated synthesis of PCs in vitro demonstrated that both genes encode PC synthase activity [1].
  • Inoculation of cad1 mutant plants with Pseudomonas syringae pv tomato DC3000 shows that the cad1 mutation results in the restriction of bacterial growth [2].
 

High impact information on CAD1

  • Cadmium-sensitive, cad1 mutants of Arabidopsis thaliana are phytochelatin deficient [3].
  • Undifferentiated cup1-1 callus tissue did not show the Cu-sensitive phenotype, suggesting that the mutant phenotype, in contrast to cad1 and cad2, is not expressed at the cellular level [4].
  • Tissue specific expression of CAD 1, B1, and G genes was determined using their promoters fused to the GUS reporter gene [5].
  • To clarify the processes involved in plant immunity, we have isolated and characterized a single recessive Arabidopsis mutant, cad1 (constitutively activated cell death 1), which shows a phenotype that mimics the lesions seen in the hypersensitive response (HR) [2].
  • We found that expression of the CAD1 gene and other W-box containing genes, such as NPR1 and PR2, was promoted by salicylic acid (SA) and benzothiadiazole (BTH) as a SA agonist [6].
 

Biological context of CAD1

  • The CAD1 gene, which encodes a protein containing a domain with significant homology to the MACPF (membrane attach complex and perforin) domain of complement components and perforin, is likely to control plant immunity negatively and has a W-box cis-element in its promoter region [6].
 

Associations of CAD1 with chemical compounds

  • Salicylic Acid and a Chitin Elicitor Both Control Expression of the CAD1 Gene Involved in the Plant Immunity of Arabidopsis [6].
  • The CAD1 expression promoted by BTH and the chitin elicitor was not suppressed in the npr1 mutant, which is insensitive to SA signaling [6].
 

Other interactions of CAD1

  • A Cu-sensitive mutant, cup1-1, of Arabidopsis thaliana has a pattern of heavy-metal sensitivity different from that of the cad1 and cad2 mutants, which are deficient in phytochelatin biosynthesis [4].
  • These results indicate that the CAD1 gene is regulated by two distinct pathways involving SA and a chitin elicitor: viz., SA signaling mediated through an NPR1-independent pathway, and chitin elicitor signaling, through an SA-independent pathway [6].
 

Analytical, diagnostic and therapeutic context of CAD1

  • Only CAD 1 protein can be detected in elongating stems, flowers, and siliques using Western-blot analysis [5].

References

  1. Phytochelatin synthase genes from Arabidopsis and the yeast Schizosaccharomyces pombe. Ha, S.B., Smith, A.P., Howden, R., Dietrich, W.M., Bugg, S., O'Connell, M.J., Goldsbrough, P.B., Cobbett, C.S. Plant Cell (1999) [Pubmed]
  2. The Arabidopsis gene CAD1 controls programmed cell death in the plant immune system and encodes a protein containing a MACPF domain. Morita-Yamamuro, C., Tsutsui, T., Sato, M., Yoshioka, H., Tamaoki, M., Ogawa, D., Matsuura, H., Yoshihara, T., Ikeda, A., Uyeda, I., Yamaguchi, J. Plant Cell Physiol. (2005) [Pubmed]
  3. Cadmium-sensitive, cad1 mutants of Arabidopsis thaliana are phytochelatin deficient. Howden, R., Goldsbrough, P.B., Andersen, C.R., Cobbett, C.S. Plant Physiol. (1995) [Pubmed]
  4. Copper-sensitive mutant of Arabidopsis thaliana. van Vliet, C., Anderson, C.R., Cobbett, C.S. Plant Physiol. (1995) [Pubmed]
  5. Evidence for a role of AtCAD 1 in lignification of elongating stems of Arabidopsis thaliana. Eudes, A., Pollet, B., Sibout, R., Do, C.T., S??guin, A., Lapierre, C., Jouanin, L. Planta (2006) [Pubmed]
  6. Salicylic Acid and a Chitin Elicitor Both Control Expression of the CAD1 Gene Involved in the Plant Immunity of Arabidopsis. Tsutsui, T., Morita-Yamamuro, C., Asada, Y., Minami, E., Shibuya, N., Ikeda, A., Yamaguchi, J. Biosci. Biotechnol. Biochem. (2006) [Pubmed]
 
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