Identification and Characterization of Thioredoxin H-Type Gene Family in Triticum turgidum ssp. durum in Response to Natural and Environmental Factor-Induced Oxidative Stress

Abstract

Key message: Thioredoxin h-type isoforms are tissue-specific, differentially expressed in germinating seeds and under salinity stress and highly regulated by H2O2, suggestive of a role in germination and salinity adaptation in durum wheat through redox regulation. Thioredoxins (Trxs) are protein-disulfide reductases that perform multiple functions related to cellular redox homoeostasis. The most complex cluster in the family of plant Trxs is formed by h-type Trxs since their identity and functions are still largely unknown. Here, h-type Trxs from durum wheat (Triticum turgidum ssp. durum) (stated TdTrxh1, TdTrxh2, TdTrxh3, and TdTrxh9) were identified and characterized in response to oxidative stress either generated naturally (germination) or induced by salinity and hydrogen peroxide (H2O2). In silico expression analysis, based on RNA-seq data, revealed a tissue-specific expression for TdTrxh genes. Real-time q-PCR analysis showed differential expression patterns for TdTrxh genes between and within seed tissues during germination and a marked induction of TdTrxh2 and h3 ones. Moreover, the four TdTrxh isoforms were found to be differentially modulated by salinity in two durum wheat varieties contrasting in their salinity tolerance. Particularly, an upregulation of the four TdTrxh genes (mainly TdTrxh2 and h3) was noted in root tissues of the tolerant variety, while they were markedly downregulated in those of the sensitive one. This upregulation of TdTrxh genes in the tolerant variety coincided with an accumulation of H2O2 in root tissues. When exogenously applied, H2O2 increased mRNA transcripts of all TdTrxh genes in both varieties regardless of their salinity-tolerance degree. Collectively, our data suggest a non-redundant function for h-type Trxs besides to be potentially involved in salinity tolerance in durum wheat through redox regulation.