Genome-wide identification, characterisation and expression profile analysis of DEAD-box family genes in sweet potato wild ancestor Ipomoea trifida under abiotic stresses

2020 ◽  
Vol 42 (3) ◽  
pp. 325-335 ◽  
Author(s):  
Rong Wan ◽  
Jingran Liu ◽  
Zhengmei Yang ◽  
Panpan Zhu ◽  
Qinghe Cao ◽  
...  
BMC Genetics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Yuxia Li ◽  
Lei Zhang ◽  
Panpan Zhu ◽  
Qinghe Cao ◽  
Jian Sun ◽  
...  

Abstract Background WRKY DNA-binding protein (WRKY) is a large gene family involved in plant responses and adaptation to salt, drought, cold and heat stresses. Sweet potato from the genus Ipomoea is a staple food crop, but the WRKY genes in Ipomoea species remain unknown to date. Hence, we carried out a genome-wide analysis of WRKYs in Ipomoea trifida (H.B.K.) G. Don., the wild ancestor of sweet potato. Results A total of 83 WRKY genes encoding 96 proteins were identified in I. trifida, and their gene distribution, duplication, structure, phylogeny and expression patterns were studied. ItfWRKYs were distributed on 15 chromosomes of I. trifida. Gene duplication analysis showed that segmental duplication played an important role in the WRKY gene family expansion in I. trifida. Gene structure analysis showed that the intron-exon model of the ItfWRKY gene was highly conserved. Meanwhile, the ItfWRKYs were divided into five groups (I, IIa + IIb, IIc, IId + IIe and III) on the basis of the phylogenetic analysis on I. trifida and Arabidopsis thaliana WRKY proteins. In addition, gene expression profiles confirmed by quantitative polymerase chain reaction showed that ItfWRKYs were highly up-regulated or down-regulated under salt, drought, cold and heat stress conditions, implying that these genes play important roles in response and adaptation to abiotic stresses. Conclusions In summary, genome-wide identification, gene structure, phylogeny and expression analysis of WRKY gene in I. trifida provide basic information for further functional studies of ItfWRKYs and for the molecular breeding of sweet potato.


PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222203 ◽  
Author(s):  
P. Maheshwari ◽  
Divya Kummari ◽  
Sudhakar Reddy Palakolanu ◽  
U. Nagasai Tejaswi ◽  
M. Nagaraju ◽  
...  

2003 ◽  
Vol 47 (4) ◽  
pp. 1220-1227 ◽  
Author(s):  
P. David Rogers ◽  
Katherine S. Barker

ABSTRACT Candida albicans is an opportunistic human fungal pathogen and a causative agent of oropharyngeal candidiasis (OPC), the most frequent opportunistic infection among patients with AIDS. Fluconazole and other azole antifungal agents have proven effective in the management of OPC; however, with increased use of these agents treatment failures have occurred. Such failures have been associated with the emergence of azole-resistant strains of C. albicans. In the present study we examined changes in the genome-wide gene expression profile of a series of C. albicans clinical isolates representing the stepwise acquisition of azole resistance. In addition to genes previously associated with azole resistance, we identified many genes whose differential expression was for the first time associated with this phenotype. Furthermore, the expression of these genes was correlated with that of the known resistance genes CDR1, CDR2, and CaMDR1. Genes coordinately regulated with the up-regulation of CDR1 and CDR2 included the up-regulation of GPX1 and RTA3 and the down-regulation of EBP1. Genes coordinately regulated with the up-regulation of CaMDR1 included the up-regulation of IFD1, IFD4, IFD5, IFD7, GRP2, DPP1, CRD2, and INO1 and the down-regulation of FET34, OPI3, and IPF1222. Several of these appeared to be coordinately regulated with both the CDR genes and CaMDR1. Many of these genes are involved in the oxidative stress response, suggesting that reduced susceptibility to oxidative damage may contribute to azole resistance. Further evaluation of the role these genes and their respective gene products play in azole antifungal resistance is warranted.


PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0123356 ◽  
Author(s):  
Chuanjun Xu ◽  
Biyu Zeng ◽  
Junmei Huang ◽  
Wen Huang ◽  
Yumei Liu

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