Stress-responsive pathways and small RNA changes distinguish variable developmental phenotypes caused by MSH1 loss.

Area of Science:

• Plant Biology
• Genetics
• Molecular Biology

Background:

• Proper regulation of nuclear-encoded, organelle-targeted genes is vital for plastid and mitochondrial function.
• MutS Homolog 1 (MSH1) is a key gene involved in generating diverse mutant phenotypes.
• MSH1 mutants exhibit stress tolerance and epigenetic changes, with severe phenotypes appearing after two generations in Arabidopsis.

Purpose of the Study:

• To investigate the generational and phenotypic differences in msh1 mutants.
• To profile the transcriptomes and small RNA populations of msh1 mutants.
• To understand the role of MSH1 in plant development and stress signaling.

Main Methods:

• RNA sequencing (RNA-seq) to analyze gene expression pathways.
• Small RNA sequencing (small RNA-seq) to identify microRNA (miRNA) and small interfering RNA (siRNA) changes.
• Comparative analysis of msh1 mutants across generations and phenotypic severity.

Main Results:

• MSH1 loss impacts pathways related to abiotic stress, pathogen defense, salicylic acid signaling, MAPK signaling, and circadian rhythm.
• Subtle redox and environment-responsive changes are observed in the first generation of msh1 mutants.
• miRNA and siRNA profiles reveal modifications in chromatin organization, with increasing changes in genes, transposable elements, and small RNAs across generations and severity.

Conclusions:

• Loss of MSH1 induces large-scale regulatory changes, integrating pathways linked to plant development and stress signaling.
• Organelles are critical integrators of internal and external cues, influencing nuclear regulation.
• Findings suggest a feedback loop between organelle status and genome regulation via small RNAs.