2019 ASHS Annual Conference

Shaolan Yang¹• Mingtong Li¹ • Suping Zhou^{2 *}

¹College of Horticulture, Qingdao Agricultural University, No. 700 Changcheng Road, Chengyang, Qingdao City 266109, Shandong Province, China；

²Department of Agricultural and Environmental Sciences, College of Agriculture, Tennessee State University, 3500 John Merritt Blvd, Nashville, TN 37209, USA

^*Authors to whom correspondence should be addressed; E-mail: zsuping@tnstate.edu (S.Z.) Abstract

A disorder in pears known as ‘hard-end’ fruit affects the appearance, edible quality, and market value of pear fruit. To explore the mechanism underlying the formation of hard-end, RNA-Seq was carried out on the calyx end of ‘Whangkeumbae’ pear fruit with and without the hard-end symptom. Results indicated that genes in the phenylpropanoid pathway affecting lignification were up-regulated in hard-end fruit. An analysis of differentially expressed genes (DEGs) identified three NAC transcription factors, and RT-qPCR analysis of PpNAC138, PpNAC186 and PpNAC187 confirmed that PpNAC187 gene expression was correlated with the hard-end disorder in pear fruit. A transient increase in PpNAC187 was observed in the calyx end of ‘Whangkeumbae’ fruit when they began to exhibit hard-end symptom. Concomitantly, a higher level of PpCCR transcripts was observed; which is a key gene in lignin biosynthesis. Notably, lignin content in the stem and leaf tissues of transgenic tobacco overexpressing PpNAC187 was significantly higher than in control plants transformed with an empty vector. Furthermore, transgenic tobacco overexpressing PpNAC187 had a larger number of xylem vessel elements. Collectively, the results of this study confirmed that PpNAC187 functions in inducing lignification in pear fruit during the development of the hard-end disorder.