ArticleMolecular and cellular biology2005
Loss of SMEK, a novel, conserved protein, suppresses MEK1 null cell polarity, chemotaxis, and gene expression defects.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- The adeno-associated virus Rep proteins target PP4:SMEK1 by preventing substrate recruitment.PLoS pathogens · 2026Article
- The triglyceride catabolism regulated by a serine/threonine protein phosphatase, Smek1, is required for development and plant infection in Magnaporthe oryzae.Molecular plant pathology · 2023Article
- Hyponastic Leaves 1 Interacts with RNA Pol II to Ensure Proper Transcription of MicroRNA Genes.Plant & cell physiology · 2023Article
- SMEK1 promotes lung adenocarcinoma proliferation and invasion by activating Wnt/β-catenin signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- An integrated, cross-regulation pathway model involving activating/adaptive and feed-forward/feed-back loops for directed oscillatory cAMP signal-relay/response during the development ofFrontiers in cell and developmental biology · 2023Article
- Ppp4r3a deficiency leads to depression-like behaviors in mice by modulating the synthesis of synaptic proteins.Disease models & mechanisms · 2022Article
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- Smek1/2 is a nuclear chaperone and cofactor for cleaved Wnt receptor Ryk, regulating cortical neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Smek promotes corticogenesis through regulating Mbd3's stability and Mbd3/NuRD complex recruitment to genes associated with neurogenesis.PLoS biology · 2017Article
- PLATINUM SENSITIVE 2 LIKE impacts growth, root morphology, seed set, and stress responses.PloS one · 2017Article
- Moving towards a paradigm: common mechanisms of chemotactic signaling in Dictyostelium and mammalian leukocytes.Cellular and molecular life sciences : CMLS · 2014Review
- Psy2 targets the PP4 family phosphatase Pph3 to dephosphorylate Mth1 and repress glucose transporter gene expression.Molecular and cellular biology · 2014Article
- Protein phosphatase 4 and Smek complex negatively regulate Par3 and promote neuronal differentiation of neural stem/progenitor cells.Cell reports · 2013Article
- PP4 dephosphorylates Maf1 to couple multiple stress conditions to RNA polymerase III repression.The EMBO journal · 2012Article
- Smek promotes histone deacetylation to suppress transcription of Wnt target gene brachyury in pluripotent embryonic stem cells.Cell research · 2011Article
- Suppressor of MEK null (SMEK)/protein phosphatase 4 catalytic subunit (PP4C) is a key regulator of hepatic gluconeogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Integration of diverse inputs in the regulation of Caenorhabditis elegans DAF-16/FOXO.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- Protein phosphatase 4 mediates localization of the Miranda complex during Drosophila neuroblast asymmetric divisions.Genes & development · 2009Article
- MEK1 and protein phosphatase 4 coordinate Dictyostelium development and chemotaxis.Molecular and cellular biology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MEK/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase signaling is imperative for proper chemotaxis. Dictyostelium mek1(-) (MEK1 null) and erk1(-) cells exhibit severe defects in cell polarization and directional movement, but the molecules responsible for the mek1(-) and erk1(-) chemotaxis defects are unknown. Here, we describe a novel, evolutionarily conserved gene and protein (smkA and SMEK, respectively), whose loss partially suppresses the mek1(-) chemotaxis phenotypes. SMEK also has MEK1-independent functions: SMEK, but not MEK1, is required for proper cytokinesis during vegetative growth, timely exit from the mound stage during development, and myosin II assembly. SMEK localizes to the cell cortex through an EVH1 domain at its N terminus during vegetative growth. At the onset of development, SMEK translocates to the nucleus via a nuclear localization signal (NLS) at its C terminus. The importance of SMEK's nuclear localization is demonstrated by our findings that a mutant lacking the EVH1 domain complements SMEK deficiency, whereas a mutant lacking the NLS does not. Microarray analysis reveals that some genes are precociously expressed in mek1(-) and erk1(-) cells. The misexpression of some of these genes is suppressed in the smkA deletion. These data suggest that loss of MEK1/ERK1 signaling compromises gene expression and chemotaxis in a SMEK-dependent manner.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.