Energy Metabolism and Auxin Signaling Disruption Underlying Stamen Identity Defects in Tobacco Cytoplasmic Male Sterility K326 (CMS K326): Integrated Transcriptomic and Metabolomic Analyses

TL;DR

This study explores how disrupted energy metabolism and auxin signaling in tobacco plants lead to stamen development defects using multiomics data.

Contribution

The integration of transcriptomic and metabolomic data reveals new insights into nuclear–cytoplasmic interactions in CMS K326.

Findings

Disrupted energy metabolism and auxin pathways are linked to stamen developmental defects in CMS K326.

Metabolites like glucose-6-phosphate and fructose-6-phosphate decrease, while succinate accumulates in CMS K326.

Deficient auxin IAA and disrupted nuclear–cytoplasmic communication contribute to stamen identity defects.

Abstract

Cytoplasmic male sterility (CMS) provides a natural model for studying nuclear–cytoplasmic interactions, although the details of nuclear–cytoplasmic communication remain poorly understood. In this study, transcriptomic and metabolomic data were integrated to elucidate the molecular and metabolic regulatory networks underlying stamen developmental defects in the tobacco CMS K326 (Nicotiana tabacum). Disrupted energy metabolism, auxin pathways, and floral development gene expression were identified in CMS K326. Metabolites such as glucose-6-phosphate, fructose-6-phosphate, and oxalosuccinic acid decreased, while an accumulation of succinate was observed and auxin IAA was deficient. Our study revealed that disrupted nuclear–cytoplasmic interactions in CMS K326 are associated with concurrent disruptions in early auxin homeostasis and energy metabolism, which collectively lead to the disturbance of the stamen development program. This study provides multiomics-level evidence for understanding stamen identity defects in CMS.

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