Yikun He

Prof. Dr. Yikun He

College of Life Sciences, Capital Normal University, Beijing 100000, China

Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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20 April 2015 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Open access
PDF file
LXLihong Xiao
Lihong Xiao
GYGe Yang
Ge Yang
LZLiechi Zhang
Liechi Zhang
XYXinhua Yang
Xinhua Yang
SZShuang Zhao
Shuang Zhao
YHYikun He
Yikun He
Significance: The genome analysis presented here represents a major step forward in the field of desiccation tolerance and a much-anticipated resource that will have a far-reaching effect in many areas of plant biology and agriculture. We present the ∼1.69-Gb draft genome of Boea hygrometrica , an important plant model for understanding responses to dehydration. To our knowledge, this is the first genome sequence of a desiccation-tolerant extremophile, offering insight into the evolution of this important trait and a first look, to our knowledge, into the genome organization of desiccation tolerance. The underpinning genome architecture and response in relation to the hydration state of the plant and its role in the preservation of cellular integrity has important implications for developing drought tolerance improvement strategies for our crops.

20 June 2016 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
SYShu Yuan
Shu Yuan
ZZZhong-Wei Zhang
Zhong-Wei Zhang
CZChong Zheng
Chong Zheng
ZZZhong-Yi Zhao
Zhong-Yi Zhao
YWYu Wang
Yu Wang
YHYikun He
Yikun He
Significance: Overapplication of nitrogen (N) fertilizer causes delayed flowering and negatively impacts the function and composition of natural ecosystems and climate. In this study, we demonstrate that flowering time variations regulated by altered nitrogen levels are mediated by two key factors: ferredoxin-NADP + -oxidoreductase (FNR1) and the blue-light receptor cryptochrome 1 (CRY1). Nitrogen regulates FNR1 expression, thereby contributing to changes in NADPH/NADP + and ATP/AMP ratios, which in turn activates adenosine monophosphate-activated protein kinase to modulate nuclear CRY1 abundance, which further acts in the N signal input pathway to affect central clock function and flowering time. A better understanding of N-regulated floral transition will offer biotechnological solutions to improve sustainable agriculture.

8 June 2020 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
GNGuoqi Niu
Guoqi Niu
QGQi Guo
Qi Guo
JWJia Wang
Jia Wang
SZShun Zhao
Shun Zhao
YHYikun He
Yikun He
LLLin Liu
Lin Liu
Two cytochrome P450 enzymes, CYP97A3 and CYP97C1, catalyze hydroxylations of the β- and ε-rings of α-carotene to produce lutein. Chirality is introduced at the C-3 atom of both rings, and the reactions are both pro-3 R –stereospecific. We determined the crystal structures of CYP97A3 in substrate-free and complex forms with a nonnatural substrate and the structure of CYP97C1 in a detergent-bound form. The structures of CYP97A3 in different states show the substrate channel and the structure of CYP97C1 bound with octylthioglucoside confirms the binding site for the carotenoid substrate. Biochemical assays confirm that the ferredoxin-NADP + reductase (FNR)–ferredoxin pair is used as the redox partner. Details of the pro-3 R stereospecificity are revealed in the retinal-bound CYP97A3 structure. Further analysis indicates that the CYP97B clan bears similarity to the β-ring–specific CYP97A clan. Overall, our research describes the molecular basis for the last steps of lutein biosynthesis.

9 August 2023 in Cell
Verified
Journal Article
Closed access
RHRuoyang Hu
Ruoyang Hu
XLXuedong Li
Xuedong Li
YHYong Hu
Yong Hu
RZRunjie Zhang
Runjie Zhang
QLQiang Lv
Qiang Lv
YHYikun He
Yikun He

29 October 2014 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Open access
PDF file
JXJinchan Xia
Jinchan Xia
DKDongdong Kong
Dongdong Kong
SXShaowu Xue
Shaowu Xue
WTWang Tian
Wang Tian
NLNan Li
Nan Li
YHYikun He
Yikun He
Significance: Nitric oxide (NO) plays key roles in coordinating plant growth and development with environmental cues. Potassium (K+) is an essential plant nutrient important for growth and stress tolerance. However, little is known about the molecular connection of NO to K+homeostasis. Through a genetic approach, this study provides a detailed regulatory mechanism of NO to K+channel AKT1-mediated K+absorption, through its modulation on vitamin B6 biosynthesis in plants. This finding demonstrates a previously unidentified role of NO in the control of K+content in plants, which may represent a normal plant adaptive response under unfavorable external conditions.

12 December 2013 in Journal of Experimental Botany
Verified
Journal Article
Open access
PDF file
JDJing Du
Jing Du
MLManli Li
Manli Li
DKDongdong Kong
Dongdong Kong
LWLei Wang
Lei Wang
QLQiang Lv
Qiang Lv
YHYikun He
Yikun He
After germination, cotyledons undertake the major role in supplying nutrients to the pre-photoautorophy angiosperm seedlings until they senesce. Like other senescence processes, cotyledon senescence is a programmed degenerative process. Nitric oxide can induce premature cotyledon senescence in Arabidopsis thaliana, yet the underlying mechanism remains elusive. A screen for genetic mutants identified the nes1 mutant, in which cotyledon senescence was accelerated by nitric oxide. Map-based cloning revealed that NES1 is allelic to a previously reported mitotic checkpoint family gene, MAD1. The nes1/mad1 mutants were restored to the wild type, in response to nitric oxide, by transforming them with pNES1::NES1. Ectopic expression of NES1 in the wild type delayed nitric oxide-mediated cotyledon senescence, confirming the repressive role of NES1. Moreover, two positive regulators of leaf senescence, the ethylene signalling component EIN2 and the transcription factor ORE1/AtNAC2/ANAC092, were found to function during nitric oxide-induced senescence in cotyledons. The block of ORE1 function delayed senescence and ectopic expression induced the process, revealing the positive role of ORE1. EIN2 was required to induce ORE1. Furthermore, the genetic interaction analysis between NES1 and ORE1 showed that the ore1 loss-of-function mutants were epistatic to nes1, suggesting the dominant role of ORE1 and the antagonistic role of NES1 during nitric oxide-induced cotyledon senescence in Arabidopsis.