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Literature summary extracted from

  • Wang, J.; Pavlyk, I.; Vedula, P.; Sterling, S.; Leu, N.A.; Dong, D.W.; Kashina, A.
    Arginyltransferase ATE1 is targeted to the neuronal growth cones and regulates neurite outgrowth during brain development (2017), Dev. Biol., 430, 41-51 .
    View publication on PubMedView publication on EuropePMC

Protein Variants

EC Number Protein Variants Comment Organism
2.3.2.8 additional information construction of a conditional mouse ATE1 knockout model (Ate1-floxed mice), phenotype, overview. Complete Ate1 knockout mice die at E12.5-E14.5 during development. Nes-Ate1 mice develope to full term and are born at the expected about 25% ratio, with the body weight and appearance at birth indistinguishable from their wild-type littermates. However, these newborn mice are visibly less active than wild-type, easily pushed away by their littermates during feeding and show no inclination to explore the environment within days after birth. These newborns exhibit dramatically reduced growth in the first days of postnatal life, likely due to their inability to compete for the mother's milk with wild-type littermates. Brain phenotypes, overview. Lack of arginylation causes defects in neurite outgrowth Mus musculus

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
2.3.2.8 cell body
-
 Mus musculus 44297
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2.3.2.8 growth cone Ate1 mRNA localized to the tips of the growth cones, likely due to zipcode-mediated targeting. Both ATE1 and arginylated beta-actin are localized at the growth cones Mus musculus 30426
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2.3.2.8 additional information ATE1 prominently localizes to the growth cones, in addition to the cell bodies. The Ate1 mRNA sequence reveals the existence of putative zipcode-binding sequences involved in mRNA targeting to the cell periphery and local translation at the growth cones Mus musculus
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Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.3.2.8 L-arginyl-tRNAArg + beta-actin Mus musculus
-
 tRNAArg + L-arginyl-[beta-actin]
-
 ?
2.3.2.8 L-arginyl-tRNAArg + protein Mus musculus
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 tRNAArg + L-arginyl-[protein]
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
2.3.2.8 Mus musculus Q9Z2A5
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
2.3.2.8 brain
-
 Mus musculus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.3.2.8 L-arginyl-tRNAArg + beta-actin
-
 Mus musculus tRNAArg + L-arginyl-[beta-actin]
-
 ?
2.3.2.8 L-arginyl-tRNAArg + protein
-
 Mus musculus tRNAArg + L-arginyl-[protein]
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.3.2.8 Ate1
-
 Mus musculus

General Information

EC Number General Information Comment Organism
2.3.2.8 malfunction conditional knockout mice with Ate1 deletion in the nervous system driven by Nestin promoter (Nes-Ate1 mice) are weaker than wild-type mice, resulting in low postnatal survival rates, and have abnormalities in the brain that suggest defects in neuronal migration. Cultured Ate1 knockout neurons show a reduction in the neurite outgrowth and the levels of doublecortin and F-actin in the growth cones. A lack of beta-actin arginylation leads to a marked reduction in growth cone spreading, accompanied by the corresponding decrease in the actin polymer. Nes-Ate1 mice develope to full term and are born at the expected about 25% ratio, with the body weight and appearance at birth indistinguishable from their wild-type littermates. However, these newborn mice are visibly less active than wild-type, easily pushed away by their littermates during feeding and show no inclination to explore the environment within days after birth. These newborns exhibit dramatically reduced growth in the first days of postnatal life, likely due to their inability to compete for the mother's milk with wild-type littermates. Complete Ate1 knockout mice die at E12.5-E14.5 during development Mus musculus
2.3.2.8 physiological function protein arginylation mediated by arginyltransferase ATE1 is an emerging regulatory modification that consists of posttranslational tRNA-mediated addition of arginine to proteins. Arginyltransferase ATE1 regulates embryogenesis and actin cytoskeleton. Role of ATE1 in brain development and neuronal growth. Zipcode-mediated co-targeting of Ate1 and beta-actin mRNA leads to localized co-translational arginylation of beta-actin that drives the growth cone migration and neurite outgrowth. The mechanism that regulates neurite outgrowth during development via arginylation and potentially involves targeted cotranslational arginylation of beta-actin in the developing growth cones, overview. ATE1 is targeted to the tips of the growing neurites where it arginylates beta-actin Mus musculus