Autophagy is an intracellular self-degradation pathway by which eukaryotic cells recycle their own material in response to specific stress conditions. Exposure to high concentrations of metals causes cell damage, although the effect of metal stress on autophagy has not been explored in photosynthetic organisms. In this study, we investigated the effect of metal excess on autophagy in the model unicellular green alga Chlamydomonas reinhardtii. We show in cells treated with nickel an upregulation of ATG8 that is independent of CRR1, a global regulator of copper signaling in Chlamydomonas. A similar effect on ATG8 was observed with copper and cobalt but not with cadmium or mercury ions. Transcriptome sequencing data revealed an increase in the abundance of the protein degradation machinery, including that responsible for autophagy, and a substantial overlap of that increased abundance with the hydrogen peroxide response in cells treated with nickel ions. Thus, our results indicate that metal stress triggers autophagy in Chlamydomonas and suggest that excess nickel may cause oxidative damage, which in turn activates degradative pathways, including autophagy, to clear impaired components and recover cellular homeostasis.
Keyphrases
- induced apoptosis
- endoplasmic reticulum stress
- cell death
- signaling pathway
- cell cycle arrest
- oxidative stress
- hydrogen peroxide
- single cell
- gene expression
- transcription factor
- reduced graphene oxide
- carbon nanotubes
- oxide nanoparticles
- stem cells
- gold nanoparticles
- rna seq
- risk assessment
- electronic health record
- poor prognosis
- climate change
- multidrug resistant
- small molecule
- dna methylation
- artificial intelligence
- metal organic framework
- antibiotic resistance genes
- microbial community
- stress induced
- big data
- gram negative
- long non coding rna
- drinking water
- fluorescent probe