Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.12.2 (MEK)
 18,161 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tobacco protein kinase NPK1 is a MAPKKK that regulates formation of the cell plate during cytokinesis. In the present study, we have identified tobacco NQK1/NtMEK1 and NRK1 as a MAPKK and a MAPK, respectively, downstream of NPK1. NQK1/NtMEK1 complements the mutation in the PBS2 MAPKK gene of yeast in a manner that depends on both NPK1 and its activator, NACK1, a kinesin-like protein. Active NPK1 and NQK1/NtMEK1 phosphorylate and activate NQK1/NtMEK1 and NRK1, respectively. Both NQK1/NtMEK1 and NRK1, as well as NPK1, are activated at the late M phase of the cell cycle in tobacco cells, and they are rapidly inactivated by depolymerization of phragmoplast microtubules. These results suggest the existence of a MAPK cascade that consists of NPK1, NQK1/NtMEK1, and NRK1 and functions in a process related to the architecture of phragmoplasts at the late M phase of the cell cycle. Overexpression of kinase-negative NQK1/NtMEK1 in tobacco cells generates multinucleate cells with incomplete cross-walls. Arabidopsis plants with a mutation in the ANQ1 gene, an ortholog of NQK1/NtMEK1, display a dwarf phenotype, with unusually large cells that contain multiple nuclei and cell-wall stubs in various organs. In addition, anq1 homozygotes set fewer flowers and produce large and malformed pollen grains with a tetrad structure. Thus, NQK1/NtMEK1 (ANQ1) MAPKK appears to be a positive regulator of plant cytokinesis during meiosis as well as mitosis.
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PMID:NQK1/NtMEK1 is a MAPKK that acts in the NPK1 MAPKKK-mediated MAPK cascade and is required for plant cytokinesis. 1270 83

The tobacco N gene, a member of the Toll-interleukin 1 homology region/nucleotide binding site/leucine-rich repeat (TIR-NBS-LRR) class of resistance (R) genes, confers resistance to tobacco mosaic virus (TMV). We used a candidate gene approach to identify known defense genes that were also involved in N signaling. The requirement for these genes was determined by downregulating their expression using the well-established tobacco rattle virus (TRV)-based virus-induced gene silencing (VIGS). Silencing of genes encoding a mitogen-activated protein kinase (MAPK) NTF6/NRK1, or an MAPK kinase (MAPKK) MEK1/NQK1, attenuated N-mediated resistance to TMV. We also found that N resistance is compromised in plants in which expression of WRKY1-WRKY3 and MYB1 transcription factors were downregulated. In addition, suppression of jasmonic acid (JA) signaling component COI1 ortholog affected N function. However, downregulation of expression of CTR1 ortholog leads to more rapid hypersensitive response (HR). The involvement of these genes in N- and other R-gene-mediated defense provides further evidence for the convergence of downstream signaling pathways of different R genes.
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PMID:Involvement of MEK1 MAPKK, NTF6 MAPK, WRKY/MYB transcription factors, COI1 and CTR1 in N-mediated resistance to tobacco mosaic virus. 1514 81