Phosphorus-induced restructuring of the ascorbate-glutathione cycle and lignin biosynthesis alleviates manganese toxicity in peach roots.
Iqra NoorHamza SohailCao WentaoKaijie ZhuMirza HasanuzzamanGuohuai LiJunwei LiuPublished in: Tree physiology (2024)
Manganese (Mn) is indispensable for plant growth, but its excessive uptake in acidic soils leads to toxicity, hampering food safety. Phosphorous (P) application is known to mitigate Mn toxicity, yet the underlying molecular mechanism remains elusive. Here, we conducted physiological and transcriptomic analyses of peach roots response to P supply under Mn toxicity. Mn treatment disrupted root architecture and caused ultrastructural damage due to oxidative injury. Notably, P application ameliorated the detrimental effects and improved the damaged roots by preventing the shrinkage of cortical cells, epidermis, and endodermis, as well as reducing the accumulation of reactive oxygen species (ROS). Transcriptomic analysis revealed the differentially expressed genes enriched in phenylpropanoid biosynthesis, cysteine, methionine, and glutathione metabolism under Mn and P treatments. P application upregulated the transcripts and activities of core enzymes crucial for lignin biosynthesis, enhancing cell wall integrity. Furthermore, P treatment activated ascorbate-glutathione cycle, augmenting ROS detoxification. Additionally, under Mn toxicity, P application downregulated Mn uptake transporter while enhancing vacuolar sequestration transporter transcripts, reducing Mn uptake and facilitating vacuolar storage. Collectively, P application prevents Mn accumulation in roots by modulating Mn transporters, bolstering lignin biosynthesis, and attenuating oxidative stress, thereby improving root growth under Mn toxicity. Our findings provide novel insights into the mechanism of P-mediated alleviation of Mn stress, and strategies for managing metal toxicity in peach orchards.
Keyphrases
- oxidative stress
- room temperature
- transition metal
- cell wall
- metal organic framework
- reactive oxygen species
- induced apoptosis
- ionic liquid
- dna damage
- cell death
- diabetic rats
- physical activity
- ischemia reperfusion injury
- climate change
- heavy metals
- risk assessment
- gene expression
- weight gain
- high glucose
- living cells
- heat stress
- sewage sludge