Altered Expression of OsAAP3 Influences Rice Lesion Mimic and Leaf Senescence by Regulating Arginine Transport and Nitric Oxide Pathway.

Qilang Wei,Zhenwei Yan,Zhongming Fang,Yifan Xiong

doi:10.3390/ijms22042181

Abstract

Persistent lesion mimic can cause leaf senescence, affecting grain yield in crops. However, knowledge about the regulation of lesion mimic and leaf senescence in crop plants is still limited. Here, we report that the amino acid transporter OsAAP3, a negative regulator of tiller bud elongation and rice grain yield, is involved in lesion mimic and leaf senescence. Altered expression of OsAAP3 can initiate the nitric oxide signaling pathway through excessive accumulation of arginine in rice leaves, influencing ROS accumulation, antioxidant enzymes activities, proline concentration, and malondialdehyde concentration. This finally triggers cell death which ultimately leads to lesion mimic and leaf senescence by regulating the degradation of chloroplast and the expression abundance of components in the photosynthetic pathway. Overall, the results not only provide initial insights into the regulatory role of amino acid transport genes in rice growth and development, but also help to understand the factors regulating the leaf senescence.

Highlights

Over-Expression of OsAAP3 Leads to Lesion Mimic and Leaf Senescence in Rice
OsAAP3 decreases the number of tillers and grain yield of rice [17], and leads to lesion mimic and leaf senescence in rice, especially in flag leaves
The results showed that the concentration of nitric oxide (NO) in the OE lines was significantly higher than that in the WT, while the NO concentration in the RNA interference (Ri) lines was significantly lower than that in the WT (Figure 1C)

Summary

Introduction

Lesion mimics refer to the disease spots spontaneously produced on plant leaves, stems, and leaf sheaths without pathogen infection or environmental stress. The formation of lesion mimics is closely related to cell development and plant defense. Some lesion mimic-related genes have been found in rice to control cell death in the defense response of pathogens. Mutant spl has been shown to affect leaf lesions and senescence in rice [2]. SPL35 plays an important role in rice cell death [3]. If lesion mimics persist, the drastic changes of leaf metabolism will lead to the degradation of metabolites and the mobilization of nutrients to developing tissues and organs, and eventually result in leaf senescence in rice [4]

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