BRENDA - Enzyme Database show

Context specificity of stress-activated mitogen-activated protein (MAP) kinase signaling: the story as told by Caenorhabditis elegans

Andrusiak, M.G.; Jin, Y.; J. Biol. Chem. 291, 7796-7804 (2016)

Data extracted from this reference:

Activating Compound
EC Number
Activating Compound
Commentary
Organism
Structure
2.7.11.24
arsenite
treatment of worms with arsenite, a toxic ROS-producing compound, induces a robust phosphorylation of PMK-1, induction of oxidative stress-responsive genes, and eventual lethality. Activation of PMK-1 following arsenite treatment is dependent on SEK-1 but independent of NSY-1, differing from the NSY-1/SEK-1/PMK-1 cascade used during infection and osmotic stress
Caenorhabditis elegans
2.7.11.24
additional information
C493C.10 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-5; jnk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-4. Activation of JNK signaling occurs under conditions of heavy metal stress; kgb-1 is phosphorylated and activated by mitogen-activated protein kinase kinase jkk-1; kgb-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-3; pmk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase mkk-4. Unique upstream components activating PMK-1 induce SKN-1 activation following toxin and bacterial exposure; pmk-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-1; pmk-3 is phosphorylated and activated by mitogen-activated protein kinase kinase mek-1
Caenorhabditis elegans
Application
EC Number
Application
Commentary
Organism
2.7.11.24
analysis
the use of 3'-UTR elements to regulate tissue-specific expression of pmk-2 provides a mechanism that endows context specificity to p38 paralogues
Caenorhabditis elegans
Engineering
EC Number
Amino acid exchange
Commentary
Organism
2.7.11.24
additional information
a kgb-1 null mutant is obtained by targeted deletion; a strain with mutations in both pmk-1 and pmk-2 is serendipitously identified in a screen searching for suppressors of the pmk-1 loss of function phenotype following bacterial infection; a strain with mutations in both pmk-1 and pmk-2 is serendipitously identified in a screen searching for suppressors of the pmk-1 loss of function phenotype following bacterial infection. Removing the 3'-UTR of pmk-2 causes its expression in the intestine, which is sufficient to rescue the Esp phenotype of pmk-1 mutants
Caenorhabditis elegans
Localization
EC Number
Localization
Commentary
Organism
GeneOntology No.
Textmining
2.7.11.24
synapse
-
Caenorhabditis elegans
45202
-
Metals/Ions
EC Number
Metals/Ions
Commentary
Organism
Structure
2.7.11.24
Mg2+
required
Caenorhabditis elegans
Natural Substrates/ Products (Substrates)
EC Number
Natural Substrates
Organism
Commentary (Nat. Sub.)
Natural Products
Commentary (Nat. Pro.)
Organism (Nat. Pro.)
Reversibility
2.7.11.24
ATP + GLH-1
Caenorhabditis elegans
-
ADP + phosphorylated GLH-1
-
-
?
Organism
EC Number
Organism
Primary Accession No. (UniProt)
Commentary
Textmining
2.7.11.24
Caenorhabditis elegans
-
-
-
2.7.11.24
Caenorhabditis elegans
H2KZI0
-
-
2.7.11.24
Caenorhabditis elegans
O44408
-
-
2.7.11.24
Caenorhabditis elegans
O44514
-
-
2.7.11.24
Caenorhabditis elegans
Q17446
-
-
2.7.11.24
Caenorhabditis elegans
Q8MXI4
-
-
2.7.11.24
Caenorhabditis elegans
Q8WQG9
-
-
Posttranslational Modification
EC Number
Posttranslational Modification
Commentary
Organism
2.7.11.24
phosphoprotein
C493C.10 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-5; jnk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-4; kgb-1 is phosphorylated and activated by mitogen-activated protein kinase kinase jkk-1; kgb-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-3; pmk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase mkk-4. Treatment of worms with arsenite, a toxic ROS-producing compound, induces a robust phosphorylation of PMK-1, induction of oxidative stress-responsive genes, and eventual lethality; pmk-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-1; pmk-3 is phosphorylated and activated by mitogen-activated protein kinase kinase mek-1
Caenorhabditis elegans
Source Tissue
EC Number
Source Tissue
Commentary
Organism
Textmining
2.7.11.24
germ cell
-
Caenorhabditis elegans
-
2.7.11.24
intestine
-
Caenorhabditis elegans
-
2.7.11.24
additional information
the enzyme shows a broad tissue expression pattern; the enzyme shows a broad tissue expression pattern; the enzyme shows a broad tissue expression pattern
Caenorhabditis elegans
-
2.7.11.24
neuron
; the enzyme is expressed in neuronal tissue; the enzyme is expressed in neuronal tissue
Caenorhabditis elegans
-
Substrates and Products (Substrate)
EC Number
Substrates
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
2.7.11.24
ATP + GLH-1
-
740759
Caenorhabditis elegans
ADP + phosphorylated GLH-1
-
-
-
?
Cofactor
EC Number
Cofactor
Commentary
Organism
Structure
2.7.11.24
ATP
-
Caenorhabditis elegans
Activating Compound (protein specific)
EC Number
Activating Compound
Commentary
Organism
Structure
2.7.11.24
arsenite
treatment of worms with arsenite, a toxic ROS-producing compound, induces a robust phosphorylation of PMK-1, induction of oxidative stress-responsive genes, and eventual lethality. Activation of PMK-1 following arsenite treatment is dependent on SEK-1 but independent of NSY-1, differing from the NSY-1/SEK-1/PMK-1 cascade used during infection and osmotic stress
Caenorhabditis elegans
2.7.11.24
additional information
jnk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-4. Activation of JNK signaling occurs under conditions of heavy metal stress
Caenorhabditis elegans
2.7.11.24
additional information
pmk-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-1
Caenorhabditis elegans
2.7.11.24
additional information
pmk-3 is phosphorylated and activated by mitogen-activated protein kinase kinase mek-1
Caenorhabditis elegans
2.7.11.24
additional information
kgb-1 is phosphorylated and activated by mitogen-activated protein kinase kinase jkk-1
Caenorhabditis elegans
2.7.11.24
additional information
kgb-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-3
Caenorhabditis elegans
2.7.11.24
additional information
pmk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase mkk-4. Unique upstream components activating PMK-1 induce SKN-1 activation following toxin and bacterial exposure
Caenorhabditis elegans
2.7.11.24
additional information
C493C.10 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-5
Caenorhabditis elegans
Application (protein specific)
EC Number
Application
Commentary
Organism
2.7.11.24
analysis
the use of 3'-UTR elements to regulate tissue-specific expression of pmk-2 provides a mechanism that endows context specificity to p38 paralogues
Caenorhabditis elegans
Cofactor (protein specific)
EC Number
Cofactor
Commentary
Organism
Structure
2.7.11.24
ATP
-
Caenorhabditis elegans
Engineering (protein specific)
EC Number
Amino acid exchange
Commentary
Organism
2.7.11.24
additional information
a strain with mutations in both pmk-1 and pmk-2 is serendipitously identified in a screen searching for suppressors of the pmk-1 loss of function phenotype following bacterial infection. Removing the 3'-UTR of pmk-2 causes its expression in the intestine, which is sufficient to rescue the Esp phenotype of pmk-1 mutants
Caenorhabditis elegans
2.7.11.24
additional information
a kgb-1 null mutant is obtained by targeted deletion
Caenorhabditis elegans
2.7.11.24
additional information
a strain with mutations in both pmk-1 and pmk-2 is serendipitously identified in a screen searching for suppressors of the pmk-1 loss of function phenotype following bacterial infection
Caenorhabditis elegans
Localization (protein specific)
EC Number
Localization
Commentary
Organism
GeneOntology No.
Textmining
2.7.11.24
synapse
-
Caenorhabditis elegans
45202
-
Metals/Ions (protein specific)
EC Number
Metals/Ions
Commentary
Organism
Structure
2.7.11.24
Mg2+
required
Caenorhabditis elegans
Natural Substrates/ Products (Substrates) (protein specific)
EC Number
Natural Substrates
Organism
Commentary (Nat. Sub.)
Natural Products
Commentary (Nat. Pro.)
Organism (Nat. Pro.)
Reversibility
2.7.11.24
ATP + GLH-1
Caenorhabditis elegans
-
ADP + phosphorylated GLH-1
-
-
?
Posttranslational Modification (protein specific)
EC Number
Posttranslational Modification
Commentary
Organism
2.7.11.24
phosphoprotein
jnk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-4
Caenorhabditis elegans
2.7.11.24
phosphoprotein
pmk-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-1
Caenorhabditis elegans
2.7.11.24
phosphoprotein
pmk-3 is phosphorylated and activated by mitogen-activated protein kinase kinase mek-1
Caenorhabditis elegans
2.7.11.24
phosphoprotein
kgb-1 is phosphorylated and activated by mitogen-activated protein kinase kinase jkk-1
Caenorhabditis elegans
2.7.11.24
phosphoprotein
kgb-2 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-3
Caenorhabditis elegans
2.7.11.24
phosphoprotein
pmk-1 is phosphorylated and activated by mitogen-activated protein kinase kinase mkk-4. Treatment of worms with arsenite, a toxic ROS-producing compound, induces a robust phosphorylation of PMK-1, induction of oxidative stress-responsive genes, and eventual lethality
Caenorhabditis elegans
2.7.11.24
phosphoprotein
C493C.10 is phosphorylated and activated by mitogen-activated protein kinase kinase sek-5
Caenorhabditis elegans
Source Tissue (protein specific)
EC Number
Source Tissue
Commentary
Organism
Textmining
2.7.11.24
germ cell
-
Caenorhabditis elegans
-
2.7.11.24
intestine
-
Caenorhabditis elegans
-
2.7.11.24
additional information
the enzyme shows a broad tissue expression pattern
Caenorhabditis elegans
-
2.7.11.24
neuron
the enzyme is expressed in neuronal tissue
Caenorhabditis elegans
-
2.7.11.24
neuron
-
Caenorhabditis elegans
-
Substrates and Products (Substrate) (protein specific)
EC Number
Substrates
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
2.7.11.24
ATP + GLH-1
-
740759
Caenorhabditis elegans
ADP + phosphorylated GLH-1
-
-
-
?
General Information
EC Number
General Information
Commentary
Organism
2.7.11.24
evolution
C493C.10 is an orthologue of mammalian JNK; jnk-1 is an orthologue of mammalian JNK; kgb-1 is an orthologue of mammalian JNK; kgb-2 is an orthologue of mammalian JNK. The JNK homologue KGB-2 shows 84% identity with KGB-1; pmk-1 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses; pmk-2 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses; pmk-3 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses
Caenorhabditis elegans
2.7.11.24
malfunction
a kgb-1 null mutant, obtained by targeted deletion, shows extra germ cells, increased number of P granules, and temperature-sensitive sterility. RNAi-mediated knockdown of glh-1 in kgb-1 mutants partially rescues the P granule number and temperature-sensitive sterility. Null mutations in vhp-1 cause larval lethality, which can be suppressed by null mutations in mlk-1, mek-1, kgb-1, dlk-1, or pmk-3; null mutations in vhp-1 cause larval lethality, which can be suppressed by null mutations in mlk-1, mek-1, kgb-1, dlk-1, or pmk-3. DLK-1/PMK-3 are identified to affect cilia length, via regulation of RAB-5 endosomes; removing the 3'-UTR of pmk-2 causes its expression in the intestine, which is sufficient to rescue the Esp phenotype of pmk-1 mutants. The Esp mutant phenotype worms show enhanced susceptibility to Pseudomonas aeruginosa that causes an intestinal infection and eventual death of the worm
Caenorhabditis elegans
2.7.11.24
metabolism
distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function. Functional redundancy of pmk-1 and pmk-2; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function. Functional redundancy of pmk-1 and pmk-2; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function. The three kinases DLK-1/MKK-4/PMK-3 constitute a linear pathway. MAK-2 is the homologue of MAPKAPK2 (MK2), and acts downstream of PMK-3. The conserved pathway, the DLK-1/MKK-4/PMK-3 cascade, activation is necessary to initiate axonal regrowth. The cascade is tightly regulated by protein ubiquitination during synapse development
Caenorhabditis elegans
2.7.11.24
physiological function
activation of JNK signaling occurs under conditions of heavy metal stress. Olfactory memory in Caenorhabditis elegans allows for the association of cues with positive or negative experiences. The loss of these memories proceeds through the UNC-43/TIR-1/NSY-1/SEK-1/JNK-1 cascade; PMK-3 acts during neuronal development. vhp-1 regulates MAP kinases in axon regeneration. svh-1 and svh-2 likely provide a layer of specificity in controlling the KGB-1/JNK pathway, independently of PMK-3 in axon injury response, crosstalk between the KGB-1 and PMK-3 cascades. The avoidance of high CO2 environments and pathogens is mediated by MOM-4/MKK-4/PMK-3 in the BAG neuron; roles for KGB-2 are in excess carbon dioxide (hypercapnia)-induced fertility defects and a slight negative role in axon injury response; the enzyme is involved in P granule formation in germ cell proliferation. KGB-1 can bind and phosphorylate GLH-1, which leads to degradation of phosphorylated GLH-1. KGB-1 activity negatively regulates GLH-1 and the steady state level of P granules to maintain fertility. vhp-1 regulates MAP kinases in axon regeneration. svh-1 and svh-2 likely provide a layer of specificity in controlling the KGB-1/JNK pathway, independently of PMK-3 in axon injury response, crosstalk between the KGB-1 and PMK-3 cascades. The aversive reaction to microbial exposure is mediated by a MLK-1/MEK-1(SEK-1)/KGB-1 pathway; the NSY-1/SEK-1/PMK-1 and PMK-2 cascade acts during neuronal development to regulate AWC asymmetry. The activation of this cascade is regulated in part by calcium, via calmodulin kinase II, as well as the conserved protein TIR-1. PMK-1 and PMK-2 act redundantly downstream of TIR-1/NSY-1/SEK-1 to induce TPH-1 expression in the ADF neuron following exposure to bacteria. Genes pmk-1 and pmk-2 function redundantly during olfactory neuronal development; the NSY-1/SEK-1/PMK-1 and PMK-2 cascade acts during neuronal development to regulate AWC asymmetry. The activation of this cascade is regulated in part by calcium, via calmodulin kinase II, as well as the conserved protein TIR-1. PMK-1 and PMK-2 act redundantly downstream of TIR-1/NSY-1/SEK-1 to induce TPH-1 expression in the ADF neuron following exposure to bacteria. Genes pmk-1 and pmk-2 function redundantly during olfactory neuronal development. Activation of PMK-1 following arsenite treatment is dependent on SEK-1 but independent of NSY-1, differing from the NSY-1/SEK-1/PMK-1 cascade used during infection and osmotic stress. Unique upstream components activating PMK-1 induce SKN-1 activation following toxin and bacterial exposure
Caenorhabditis elegans
General Information (protein specific)
EC Number
General Information
Commentary
Organism
2.7.11.24
evolution
jnk-1 is an orthologue of mammalian JNK
Caenorhabditis elegans
2.7.11.24
evolution
pmk-2 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses
Caenorhabditis elegans
2.7.11.24
evolution
pmk-3 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses
Caenorhabditis elegans
2.7.11.24
evolution
kgb-1 is an orthologue of mammalian JNK
Caenorhabditis elegans
2.7.11.24
evolution
kgb-2 is an orthologue of mammalian JNK. The JNK homologue KGB-2 shows 84% identity with KGB-1
Caenorhabditis elegans
2.7.11.24
evolution
pmk-1 is an orthologue of mammalian p38. The three pmk genes pmk1, pmk-2, and pmk-3, are encoded by a single polycistronic transcript (operon), precluding the generation of double mutants by traditional genetic crosses
Caenorhabditis elegans
2.7.11.24
evolution
C493C.10 is an orthologue of mammalian JNK
Caenorhabditis elegans
2.7.11.24
malfunction
null mutations in vhp-1 cause larval lethality, which can be suppressed by null mutations in mlk-1, mek-1, kgb-1, dlk-1, or pmk-3. DLK-1/PMK-3 are identified to affect cilia length, via regulation of RAB-5 endosomes
Caenorhabditis elegans
2.7.11.24
malfunction
a kgb-1 null mutant, obtained by targeted deletion, shows extra germ cells, increased number of P granules, and temperature-sensitive sterility. RNAi-mediated knockdown of glh-1 in kgb-1 mutants partially rescues the P granule number and temperature-sensitive sterility. Null mutations in vhp-1 cause larval lethality, which can be suppressed by null mutations in mlk-1, mek-1, kgb-1, dlk-1, or pmk-3
Caenorhabditis elegans
2.7.11.24
malfunction
removing the 3'-UTR of pmk-2 causes its expression in the intestine, which is sufficient to rescue the Esp phenotype of pmk-1 mutants. The Esp mutant phenotype worms show enhanced susceptibility to Pseudomonas aeruginosa that causes an intestinal infection and eventual death of the worm
Caenorhabditis elegans
2.7.11.24
metabolism
the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function
Caenorhabditis elegans
2.7.11.24
metabolism
the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function. Functional redundancy of pmk-1 and pmk-2
Caenorhabditis elegans
2.7.11.24
metabolism
the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview. Distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function. The three kinases DLK-1/MKK-4/PMK-3 constitute a linear pathway. MAK-2 is the homologue of MAPKAPK2 (MK2), and acts downstream of PMK-3. The conserved pathway, the DLK-1/MKK-4/PMK-3 cascade, activation is necessary to initiate axonal regrowth. The cascade is tightly regulated by protein ubiquitination during synapse development
Caenorhabditis elegans
2.7.11.24
metabolism
distinct p38 and JNK MAPK cascades regulate a diverse class of normal biological processes during development and nervous system function; the core MAPK signaling cassette consists of a MAPKKK/MAPKK/MAPK cascade, stress-activated MAPK components involved in non-stress-associated processes, overview
Caenorhabditis elegans
2.7.11.24
physiological function
activation of JNK signaling occurs under conditions of heavy metal stress. Olfactory memory in Caenorhabditis elegans allows for the association of cues with positive or negative experiences. The loss of these memories proceeds through the UNC-43/TIR-1/NSY-1/SEK-1/JNK-1 cascade
Caenorhabditis elegans
2.7.11.24
physiological function
the NSY-1/SEK-1/PMK-1 and PMK-2 cascade acts during neuronal development to regulate AWC asymmetry. The activation of this cascade is regulated in part by calcium, via calmodulin kinase II, as well as the conserved protein TIR-1. PMK-1 and PMK-2 act redundantly downstream of TIR-1/NSY-1/SEK-1 to induce TPH-1 expression in the ADF neuron following exposure to bacteria. Genes pmk-1 and pmk-2 function redundantly during olfactory neuronal development
Caenorhabditis elegans
2.7.11.24
physiological function
PMK-3 acts during neuronal development. vhp-1 regulates MAP kinases in axon regeneration. svh-1 and svh-2 likely provide a layer of specificity in controlling the KGB-1/JNK pathway, independently of PMK-3 in axon injury response, crosstalk between the KGB-1 and PMK-3 cascades. The avoidance of high CO2 environments and pathogens is mediated by MOM-4/MKK-4/PMK-3 in the BAG neuron
Caenorhabditis elegans
2.7.11.24
physiological function
the enzyme is involved in P granule formation in germ cell proliferation. KGB-1 can bind and phosphorylate GLH-1, which leads to degradation of phosphorylated GLH-1. KGB-1 activity negatively regulates GLH-1 and the steady state level of P granules to maintain fertility. vhp-1 regulates MAP kinases in axon regeneration. svh-1 and svh-2 likely provide a layer of specificity in controlling the KGB-1/JNK pathway, independently of PMK-3 in axon injury response, crosstalk between the KGB-1 and PMK-3 cascades. The aversive reaction to microbial exposure is mediated by a MLK-1/MEK-1(SEK-1)/KGB-1 pathway
Caenorhabditis elegans
2.7.11.24
physiological function
roles for KGB-2 are in excess carbon dioxide (hypercapnia)-induced fertility defects and a slight negative role in axon injury response
Caenorhabditis elegans
2.7.11.24
physiological function
the NSY-1/SEK-1/PMK-1 and PMK-2 cascade acts during neuronal development to regulate AWC asymmetry. The activation of this cascade is regulated in part by calcium, via calmodulin kinase II, as well as the conserved protein TIR-1. PMK-1 and PMK-2 act redundantly downstream of TIR-1/NSY-1/SEK-1 to induce TPH-1 expression in the ADF neuron following exposure to bacteria. Genes pmk-1 and pmk-2 function redundantly during olfactory neuronal development. Activation of PMK-1 following arsenite treatment is dependent on SEK-1 but independent of NSY-1, differing from the NSY-1/SEK-1/PMK-1 cascade used during infection and osmotic stress. Unique upstream components activating PMK-1 induce SKN-1 activation following toxin and bacterial exposure
Caenorhabditis elegans