Abstract

The NAC family is one of the largest families of plant-specific transcription factors (TFs) and NAC proteins play important regulatory roles in a variety of developmental and stress response processes in plants. Members of the NAC family TFs have been shown to be important regulators of leaf senescence in a number of plant species. Here we report the identification of the NAC family in tobacco (Nicotiana tabacum) and characterization of the potential role of some of the tobacco NAC TFs in regulating leaf senescence. A total of 154 NAC genes (NtNACs) were identified and clustered together with the Arabidopsis NAC family into fifteen groups (a-o). Transcriptome data analysis followed by qRT-PCR validation showed that the majority of the senescence-up-regulated NtNACs fall into subgroups NAC-b and f. A number of known senescence regulators from Arabidopsis also belong to these two subgroups. Among these senescence-up-regulated NtNACs, NtNAC080, a close homolog of AtNAP, is a positive regulator of leaf senescence. Overexpression of NtNAC080 caused early senescence in Arabidopsis leaves and NtNAC080 mutation induced by Cas9/gRNA in tobacco led to delayed leaf senescence.

Highlights

  • Senescence is the final stage of leaf development and is critical for plants’ life cycle

  • To identify NAC genes in tobacco, Hidden Markov Model (HMM) search was performed against the Sol Genomics Network database8 using the Pfam NAC domain (PF02365) as query

  • The functions of a number of NAC genes have been investigated in Arabidopsis and model crops (Guo and Gan, 2006; Garapati et al, 2015; Pimenta et al, 2016; Mao et al, 2017), little is known about this gene family in the economic crop Nicotiana tabacum

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Summary

Introduction

Senescence is the final stage of leaf development and is critical for plants’ life cycle. Previous studies have identified a number of TFs that participated in the process of leaf senescence from a number of protein families such as NAC, WRKY, and MYB proteins. These TF proteins act as switches to cause differential gene expression by binding to specific cis-acting elements of target gene promoters, resulting in the activation and/or suppression of target genes during senescence (Gregersen and Holm, 2007; Balazadeh et al, 2008; Besseau et al, 2012; Zhang and Gan, 2012; Shah et al, 2013)

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