3.4.24.B20: FtsH protease
This is an abbreviated version!
For detailed information about FtsH protease, go to the full flat file.
Word Map on EC 3.4.24.B20
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3.4.24.B20
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chloroplast
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photosystem
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thylakoids
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variegation
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photodamaged
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photoinhibition
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sigma32
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ftsh-mediated
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rpoh
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grana
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lpxc
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photoinhibitory
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ftsh-dependent
- 3.4.24.B20
- chloroplast
-
photosystem
- thylakoids
-
variegation
-
photodamaged
-
photoinhibition
- sigma32
-
ftsh-mediated
- rpoh
-
grana
- lpxc
-
photoinhibitory
-
ftsh-dependent
Reaction
degradative cleavage of proteins =
Synonyms
AAA protease, AtFtsH, AtFtsH2, AtFtsH5, AtFtsH6, ATP-dependent zinc metalloprotease, filamentation temperature sensitive H, filamentation temperature sensitive H protease, FtsH, FtsH (slr0228), FtsH metalloprotease, FtsH protease, FtsH protease slr0228, FtsH1, FtsH10, FtsH11, FtsH12, FtsH2, FtsH2 protease, FtsH3, FtsH4, FtsH5, FtsH6, FtsH7, FtsH8, FtsH9, FTSHA, FtsHB, HflB, M41.005, More, putative cell division protein, RISP-degrading activity, slr0228, VAR1, VAR2, zinc dependent protease, ZmFtsH2A, ZmFtsH2B
ECTree
3.4.24.B20 FtsH proteaseAdvanced search results
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results (Engineering
Engineering on EC 3.4.24.B20 - FtsH protease
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
H417L
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the mutant accumulates about 20% relative to the wild type enzyme and does not cleave delta32 protein
H488L
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the FtsH2 mutation inhibits zinc binding and inactivates proteolysis
A359V
homolog of the human pathogenic A510V mutation of paraplegin (SPG7), does not affect the dynamic behavior of the protease but impairs the ATP-coupled domain compaction
G404L
site-directed mutagenesis, the mutant is monomeric and inactive in the ATPase assay and possesses only very low proteolytic activity
A359V
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homolog of the human pathogenic A510V mutation of paraplegin (SPG7), does not affect the dynamic behavior of the protease but impairs the ATP-coupled domain compaction
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additional information
additional information
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a FtsH11 null mutant (salk033047) displays thermosensitive phenotypes using both acquired and basal thermotolerance assays
additional information
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ectopic expression of cGPA1 rescues the leaf variegation of ftsh2 and partially corrects mis-regulated gene expression in thf1, the leaf-variegated mutant thylakoid formation 1, phenotype, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the cells in green sectors of variegation mutant var2 have normal-appearing chloroplasts whereas cells in the white sectors have abnormal plastids that lack pigments and organized lamellae. The mutant serves as threshold model in which the formation of chloroplasts is due to the presence of activities/processes that are able to compensate for a lack of VAR2, mechanisms of variegation suppression, including an unexpected link between var2 variegation and chloroplast translation, phenotype and mutant screening, detailed overview. The enhancement in green sector formation is accompanied by an increased accumulation of chloroplast FtsH mRNA and protein. Overexpressionj of isozyme AtFtsH8 suppresses the var2 phenotype. Isolation and analysis of mutant svr1-1, i.e. suppression of variegation1-1, and of svr2 mutant, overview. Examples of var2 suppressors are clpC2, fug1, sco1, and GPA1, mutational effets, overview
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH1 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH10 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH3 shows reduced activity of mitochondrial complex I and V
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows altered late rosette leaf development and chloroplasts and mitochondria ultrastructure under short-day conditions
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH4 shows no visible phenotype, but is unable to degrade LHC II
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH5 shows variegated leaves, overexpression of isozyme AtFtsH1 suppresses the var1 phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
the knockout mutant of gene AtFtsH8 shows no visible phenotype
additional information
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generation of ftsH knockouts, that show a sporulation frequency reduced by several orders of magnitude. The combination of ftsH knockout with knockout of one of the phosphatases RapA, RapB, RapE or Spo0E results in a sporulation frequency, that is increased by two to three orders of magnitude, but still remains below 1% of wild-type level, overview
additional information
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mutants lacking 5 or 10 amino acid residues in the exposed N-terminal region of the D1 protein are blocked in the synthesis of D1 protein, photosystem II repair and selective D1 degradation are inhibited in the A20 truncation mutant
additional information
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insertional inactivation of two of the four genes, slr1390 and slr1604, is lethal, while inactivation of sll1463 does not have an obvious affect and inactivation of slr0228 produces cells with altered pigmentation and a significant reduction in the amount of PSI
