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Embryo Injection Technique for Gene Editing in the Black-Legged Tick, Ixodes scapularis
Published on: September 13, 2022
p53-associated metabolic checkpoint regulation in a tick embryo-derived cell line.
Bruno Moraes1, Angélica Arcanjo1, Tomohiro Okagawa2
1Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, RJ, Brazil.
Insect Biochemistry and Molecular Biology
|July 15, 2026
Summary
PRIMA-1 induces apoptosis in cattle tick cells by altering metabolism. This drug restricts glycolysis and the pentose phosphate pathway, reducing NADPH and reshaping redox balance, similar to effects seen in mammals.
Area of Science:
- Metabolomics
- Cell Biology
- Arthropod Biology
Background:
- The tumor suppressor protein p53 regulates genome integrity and metabolism in mammals.
- p53's metabolic roles in early-diverging metazoans are not well understood.
- Investigating p53-related metabolic pathways in arthropods can reveal conserved biological mechanisms.
Purpose of the Study:
- To investigate the metabolic responses of cattle tick embryonic cells (BME26) to PRIMA-1.
- To determine the mechanism by which PRIMA-1 affects cell viability and metabolism in Rhipicephalus microplus.
- To explore potential conserved metabolic pathways between arthropods and mammals.
Main Methods:
- BME26 cells were treated with PRIMA-1.
- Cell viability was assessed using Annexin V/7-AAD staining and morphological analysis.
- Metabolomic profiling was performed using 1H-13C HSQC NMR.
- Gene expression of key metabolic enzymes (HK, PK, G6PDH, IDH-1) was analyzed.
Main Results:
- PRIMA-1 reduced BME26 cell viability in a dose- and time-dependent manner, inducing apoptosis.
- Metabolomic profiling revealed significant remodeling of central carbon metabolism, amino acid, and choline pathways.
- PRIMA-1 decreased the expression of glycolytic genes (HK, PK) and G6PDH, leading to reduced intracellular NADPH levels.
- Isocitrate dehydrogenase-1 (IDH-1) gene expression was unaffected, indicating pathway-specific modulation.
Conclusions:
- PRIMA-1 treatment in tick cells restricts glycolytic and pentose phosphate pathway flux.
- The drug limits NADPH production and reshapes redox balance, promoting apoptosis.
- Findings suggest conserved PRIMA-1-sensitive metabolic pathways between arthropods and mammals, potentially involving the p53-G6PDH-NADPH axis.
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