High-temperature stress in crops: male sterility, yield loss and potential remedy approaches

Abstract

Global food security is one of the utmost essential challenges in the 21st century in providing enough food for the growing population while coping with the already stressed environment. High temperature (HT) is one of the main factors affecting plant growth, development and reproduction and causes male sterility in plants. In male reproductive tissues, metabolic changes induced by HT involve carbohydrates, lipids, hormones, epigenetics and reactive oxygen species, leading to male sterility and ultimately reducing yield. Understanding the mechanism and genes involved in these pathways during the HT stress response will provide a new path to improve crops by using molecular breeding and biotechnological approaches. Moreover, this review provides insight into male sterility and integrates this with suggested strategies to enhance crop tolerance under HT stress conditions at the reproductive stage.

Keywords: epigenetics; high temperature; jasmonic acid; male sterility; yield loss.

Figure 1

Increase of 1 °C temperature effect on crop yield in different countries of the world. Different colour of countries on the map shows the highest reduction in the yield of different crops in the specific country. [Correction added on 30 November 2022, after first online publication: Subfigures have been clarified in this version.]

Figure 2

Model for the function of different pathways in creating male sterility during HT stress in anther. HT affects the carbohydrate content in the anthers. The enzyme starch phosphorylase converts the carbohydrate to sugar and glucose, which disrupts the normal sugar balance process and affects the fatty acid and hormone pathways such as auxin, gibberellin and jasmonic acid. In the fatty acid pathway, the acyl‐CoA oxidase family genes, while in the alpha‐linolenic acid pathway, the acyl‐CoA oxide and allene oxide cyclase family genes were suppressed, leading to the reduced amount of jasmonic acid. In pollen grains, the disrupted hormones increased the ROS signal, which increased the programmed cell death (PCD), affected the pollen grain spikes, promoted pollen abortion and caused male sterility. In anthers, during HT stress, an increased amount of ROS reduces the antioxidant, disrupts the natural process of lignification and promotes the anther indehiscence, which leads to male sterility. Moreover, HT also disrupted DNA methylation, which affects the miRNA (miRNA160), suppressed the ARF10 and ARF17 gene, decreased the hormone (auxin), increased the ROS, promoted the anther indehiscence, pollen abortion and caused male sterility. 3‐KAT, 3‐ketoacyl‐acyl carrier protein synthaseI; ABA, Abscisic acid; ACC1, Acetyl‐CoA Carboxylase1; ACO2, Acyl‐CoA oxidase2; AOC2, Allene oxide cyclase2; AOS, Allene oxide synthase; ARF, Auxin response factor; CHH, Hyper‐CHH methylation; ER stress, Endoplasmic reticulum stress; GA, Gibberellic acid; IAA, Indole‐3‐acetic acid; JAZ, Jasmonate‐zim domain; MFP2, Multifunctional protein2; PCD, Programmed cell death; PhyB, Phytochrome B; PIF4, Phytochrome‐integrating factor 4; ROS, Reactive oxygen species; YUC8, YUCCA.

Figure 3

Model for the function of epigenetics in HT‐tolerant and sensitive line during HT stress condition in anther. (a) Epigenetic effect on HT‐tolerant line during HT stress condition. (b) Epigenetic effect on HTsensitive line during HT stress condition. ARF17, Auxin response factor17; DRM1, DNA methyl‐transferases1; DRM3, DNA methyltransferases3; HDA9, histone deacetylase 9; PCD, Programmed cell death; PWR, POWERDRESS; ROS, Reactive oxygen species; SAHH1, S‐ADENOSYL‐L‐ HOMOCYSTEINEHYDROLASE1; YUC8, YUCCA8.

Figure 4

Role of microRNA (miR159/160) in different crops and its effects on anther wall to create male sterility. microRNA activates the different proteins in various crops, affecting the endothecium wall and creating male sterility.

Figure 5

Potential remedy approaches to improving HT stress tolerance in crops.