How Histone Acetyltransferases Shape Plant Photomorphogenesis and UV Response.
Irina BoychevaGeorgi BonchevVasilissa ManovaLubomir StoilovValya VassilevaPublished in: International journal of molecular sciences (2024)
Higher plants have developed complex mechanisms to adapt to fluctuating environmental conditions with light playing a vital role in photosynthesis and influencing various developmental processes, including photomorphogenesis. Exposure to ultraviolet (UV) radiation can cause cellular damage, necessitating effective DNA repair mechanisms. Histone acetyltransferases (HATs) play a crucial role in regulating chromatin structure and gene expression, thereby contributing to the repair mechanisms. HATs facilitate chromatin relaxation, enabling transcriptional activation necessary for plant development and stress responses. The intricate relationship between HATs, light signaling pathways and chromatin dynamics has been increasingly understood, providing valuable insights into plant adaptability. This review explores the role of HATs in plant photomorphogenesis, chromatin remodeling and gene regulation, highlighting the importance of chromatin modifications in plant responses to light and various stressors. It emphasizes the need for further research on individual HAT family members and their interactions with other epigenetic factors. Advanced genomic approaches and genome-editing technologies offer promising avenues for enhancing crop resilience and productivity through targeted manipulation of HAT activities. Understanding these mechanisms is essential for developing strategies to improve plant growth and stress tolerance, contributing to sustainable agriculture in the face of a changing climate.
Keyphrases
- dna damage response
- dna repair
- gene expression
- dna damage
- dna methylation
- climate change
- plant growth
- transcription factor
- genome wide
- genome editing
- crispr cas
- oxidative stress
- cell wall
- radiation induced
- risk assessment
- depressive symptoms
- heat stress
- social support
- cancer therapy
- epithelial mesenchymal transition
- induced apoptosis