mek-1

UniProt ID: Q7RYZ6
Organism: Neurospora crassa (strain ATCC 24698 / 74-OR23-1A / CBS 708.71 / DSM 1257 / FGSC 987)
Review Status: COMPLETE
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Gene Description

MEK-1 is the MAP kinase kinase of the Neurospora crassa MIK-1–MEK-1–MAK-1 signaling module. It is required for MAK-1 phosphorylation and helps control cell wall integrity, vegetative growth, asexual development and sexual differentiation. MEK-1 also accumulates at the contact sites of fusing germlings, linking this signaling module to local remodeling during cell fusion.

Existing Annotations Review

GO Term Evidence Action Reason
GO:0000165 MAPK cascade
IEA
GO_REF:0000117
ACCEPT
Summary: MEK-1 is the middle kinase of the experimentally characterized MIK-1–MEK-1–MAK-1 cascade.
Reason: MEK-1 is the middle kinase of the experimentally characterized MIK-1–MEK-1–MAK-1 cascade. The broad MAPK cascade annotation is correct but less informative than the cell integrity cascade assignment.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0000166 nucleotide binding
IEA
GO_REF:0000104
ACCEPT
Summary: The protein kinase ATP-binding site and active catalytic domain support ATP-dependent phosphotransfer.
Reason: The protein kinase ATP-binding site and active catalytic domain support ATP-dependent phosphotransfer. Nucleotide binding is broad but true for this kinase.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0000196 cell integrity MAPK cascade
IBA
GO_REF:0000033
ACCEPT
Summary: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant.
Reason: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant. The MIK-1–MEK-1–MAK-1 module regulates fungal development and cell wall integrity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0000196 cell integrity MAPK cascade
IEA
GO_REF:0000107
ACCEPT
Summary: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant.
Reason: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant. The MIK-1–MEK-1–MAK-1 module regulates fungal development and cell wall integrity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0000935 division septum
IEA
GO_REF:0000107
UNDECIDED
Summary: The direct microscopy study locates MEK-1 at contacts between fusing germlings, which is not equivalent to a division septum.
Reason: The direct microscopy study locates MEK-1 at contacts between fusing germlings, which is not equivalent to a division septum. The fission-yeast ortholog transfer may be valid, but a target-specific septal localization or convincing conservation of that precise pattern remains unresolved.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0004672 protein kinase activity
IEA
GO_REF:0000120
ACCEPT
Summary: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity.
Reason: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity. These broad kinase or transferase terms are correct; MAP kinase kinase activity states the biological specificity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0004674 protein serine/threonine kinase activity
IEA
GO_REF:0000120
ACCEPT
Summary: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity.
Reason: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity. These broad kinase or transferase terms are correct; MAP kinase kinase activity states the biological specificity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0004707 MAP kinase activity
IEA
GO_REF:0000003
MODIFY
Summary: The EC-derived row calls MEK-1 a MAP kinase, but primary experiments distinguish MEK-1 (MAPKK) from its downstream MAPK MAK-1.
Reason: The EC-derived row calls MEK-1 a MAP kinase, but primary experiments distinguish MEK-1 (MAPKK) from its downstream MAPK MAK-1. GO:0004708 captures phosphorylation of a MAPK substrate, the appropriate kinase tier for this protein.
Proposed replacements: MAP kinase kinase activity
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0004708 MAP kinase kinase activity
IBA
GO_REF:0000033
ACCEPT
Summary: MEK-1 is the MAP kinase kinase, and MAK-1 phosphorylation depends on it in Neurospora.
Reason: MEK-1 is the MAP kinase kinase, and MAK-1 phosphorylation depends on it in Neurospora. The target kinase-domain architecture and MAPKK phylogenetic placement agree with this pathway position.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0004708 MAP kinase kinase activity
IEA
GO_REF:0000107
ACCEPT
Summary: MEK-1 is the MAP kinase kinase, and MAK-1 phosphorylation depends on it in Neurospora.
Reason: MEK-1 is the MAP kinase kinase, and MAK-1 phosphorylation depends on it in Neurospora. The target kinase-domain architecture and MAPKK phylogenetic placement agree with this pathway position.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0005524 ATP binding
IEA
GO_REF:0000120
ACCEPT
Summary: The protein kinase ATP-binding site and active catalytic domain support ATP-dependent phosphotransfer.
Reason: The protein kinase ATP-binding site and active catalytic domain support ATP-dependent phosphotransfer. Nucleotide binding is broad but true for this kinase.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0005737 cytoplasm
IEA
GO_REF:0000107
ACCEPT
Summary: The conserved fungal MAPKK localization inference is compatible with direct Neurospora microscopy showing MEK-1 recruitment to germling contact sites.
Reason: The conserved fungal MAPKK localization inference is compatible with direct Neurospora microscopy showing MEK-1 recruitment to germling contact sites. Cytoplasm is a broad compartment that includes this cortical signaling pool; the experiment does not imply uniform distribution.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0016301 kinase activity
IEA
GO_REF:0000104
ACCEPT
Summary: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity.
Reason: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity. These broad kinase or transferase terms are correct; MAP kinase kinase activity states the biological specificity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0016740 transferase activity
IEA
GO_REF:0000104
ACCEPT
Summary: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity.
Reason: The conserved catalytic protein kinase domain and experimentally established MAPKK function support phosphorylation activity. These broad kinase or transferase terms are correct; MAP kinase kinase activity states the biological specificity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0050850 positive regulation of calcium-mediated signaling
IEA
GO_REF:0000107
UNDECIDED
Summary: The transferred positive regulation of calcium-mediated signaling is more specific than the demonstrated cell integrity MAPK cascade.
Reason: The transferred positive regulation of calcium-mediated signaling is more specific than the demonstrated cell integrity MAPK cascade. Calcium-sensitive fusion phenotypes or downstream CSR-3 behavior do not establish that MEK-1 positively regulates calcium signaling itself.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).
GO:0060237 regulation of fungal-type cell wall organization
IBA
GO_REF:0000033
ACCEPT
Summary: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant.
Reason: Primary Neurospora experiments identify MEK-1 as the MAPKK upstream of MAK-1 and show loss of MAK-1 phosphorylation in the deletion mutant. The MIK-1–MEK-1–MAK-1 module regulates fungal development and cell wall integrity.
Supporting Evidence:
PMID:18849472
The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
PMID:41071819
In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).

Core Functions

MEK-1 is the MAP kinase kinase of the Neurospora crassa MIK-1–MEK-1–MAK-1 signaling module.

Molecular Function:
MAP kinase kinase activity
Directly Involved In:
Cellular Locations:
Supporting Evidence:
  • PMID:18849472
    The MAK-1 MAPK was not phosphorylated in Ξ” mik-1 and Ξ” mek-1 mutants, consistent with the involvement of MIK-1, MEK-1, and MAK-1 in the same signaling cascade.
  • PMID:41071819
    In a first step, we confirmed the accumulation of the kinase MAK-1 at the contact sites and showed the same localization pattern for both its upstream kinases (Fig 7).

References

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Deep Research

Falcon

(mek-1-deep-research-falcon.md)

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πŸ“š Additional Documentation

Notes

(mek-1-notes.md)

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Protnlm Location Review

(mek-1-protnlm-location-review.md)

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πŸ“„ View Raw YAML

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