Apr 30, 2020

The CRISPR-Cas9 crATIC HeLa transcriptome: Characterization of a novel cellular model for ATIC deficiency and ZMP accumulation

BioRxiv : the Preprint Server for Biology
R. C. MazzarinoGuido N. Vacano

Abstract

In de novo purine biosynthesis (DNPS), 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase (2.1.2.3) / inosine monophosphate cyclohydrolase (3.5.4.10) (ATIC) catalyzes the last two reactions of the pathway: conversion of 5-aminoimidazole-4-carboxamide ribonucleotide [aka Z-nucleotide monophosphate (ZMP)] to 5-formamido-4-imidazolecarboxamide ribonucleotide (FAICAR) then to inosine monophosphate (IMP). ZMP is an adenosine monophosphate (AMP) mimetic and a known activator of AMP-activated protein kinase (AMPK). Recently, a HeLa cell line null mutant for ATIC was constructed via CRISPR-Cas9 mutagenesis. This mutant, crATIC, accumulates ZMP during purine starvation. Given that the mutant can accumulate ZMP in the absence of treatment with exogenous compounds, crATIC is likely an important cellular model for DNPS inactivation and ZMP accumulation. In the current study, we characterize the crATIC transcriptome versus the HeLa transcriptome in purine-supplemented and purine-depleted growth conditions. We report and discuss transcriptome changes with particular relevance to Alzheimers disease and in genes relevant to lipid and fatty acid synthesis, neurodevelopment, embryogenesis, cell cycle maintenance and progression, ext...Continue Reading

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Mentioned in this Paper

Study
Ventricular beta-Myosin
IMMT
Actins
Hypertrophic Cardiomyopathy
Motor protein
Hyperactive Behavior
Myosin Phosphatase Myosin Binding
Contraction (Finding)
Persons

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