Yan Liang

Shanghai University, Shanghai, Shanghai Shi, China

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Publications (11)62.45 Total impact

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    ABSTRACT: In higher plants, seed germination is followed by postgerminative growth. One of the key developmental events during postgerminative growth is cotyledon greening that enables a seedling establish the photosynthetic capacity. The plant phytohormone abscisic acid (ABA) plays a vital role by inhibiting seed germination and postgerminative growth in response to the dynamically changing internal and environmental cues. It has been shown that ABSCISIC ACID INSENSITIVE 5 (ABI5), a bZIP transcription factor, is an important factor in the regulation of ABA-mediated inhibitory effect on seed germination and postgerminative growth. Conversely, the phytohormone cytokinin has been proposed to promote seed germination by antagonizing ABA-mediated inhibitory effect. However, the underpinning molecular mechanism of the cytokinin-repressed ABA signaling is largely unknown. Here, we show that cytokinin specifically antagonizes ABA-mediated inhibition on cotyledon greening with minimal effects on seed germination in Arabidopsis (Arabidopsis thaliana). We found that the cytokinin-antagonized ABA effect is dependent on a functional cytokinin signaling pathway, mainly involved in the cytokinin receptor gene CRE1/AHK4, downstream AHP2, 3, 5 genes, and a type-B response regulator gene ARR12, which genetically acts upstream of ABI5 to regulate cotyledon greening. Cytokinin has no apparent effect on the transcription of ABI5. However, cytokinin efficiently promotes the proteasomal degradation of ABI5 protein in a cytokinin signaling-dependent manner. These results define a genetic pathway, through which cytokinin specifically induces the degradation of ABI5 protein, thereby antagonizing ABA-mediated inhibition on postgerminative growth.
    Plant physiology 01/2014; · 6.56 Impact Factor
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    ABSTRACT: Nuclear factor Y (NF-Y) is a highly conserved transcription factor presented in all eukaryotic organisms, and is a heterotrimer consisting of three subunits: NF-YA, NF-YB, and NF-YC. In Arabidopsis, these three subunits are encoded by multigene families. The best-studied member of the NF-Y transcription factors is LEAFY COTYLEDON1 (LEC1), a NF-YB family member, which plays a critical role in embryogenesis and seed maturation. However, the function of most NF-Y genes remains elusive. Here, we report the characterization of four genes in the NF-YA family. We found that a gain-of-function mutant of NF-YA1 showed defects in male gametogenesis and embryogenesis. Consistently, overexpression of NF-YA1, 5, 6, and 9 affects male gametogenesis, embryogenesis, seed morphology, and seed germination, with a stronger phenotype when overexpressing NF-YA1 and NF-YA9. Moreover, overexpression of these NF-YA genes also causes hypersensitivity to abscisic acid (ABA) during seed germination, retarded seedling growth, and late flowering at different degrees. Intriguingly, overexpression of NF-YA1, 5, 6, and 9 is sufficient to induce the formation of somatic embryos from the vegetative tissues. However, single or double mutants of these NF-YA genes do not have detectable phenotype. Collectively, these results provide evidence that NF-YA1, 5, 6, and 9 play redundant roles in male gametophyte development, embryogenesis, seed development, and post-germinative growth.
    Molecular Plant 08/2012; · 6.13 Impact Factor
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    ABSTRACT: Endometriosis (EM) is highly associated with infertility. The precise mechanism underlying EM-associated infertility remains controversial. This study aimed to investigate the pathogenesis of infertility in women with EM by comparing FoxP3+ T regulatory cells (Tregs) expression in the eutopic endometrium of infertile women with EM and endometrium from healthy fertile women. As a marker of Tregs, FoxP3 expression was analyzed in eutopic endometrium during the peri-implantation phase in infertile women with mild EM (n = 7), advanced EM (n = 20), and normally fertile women without EM (n = 20). FoxP3 mRNA expression was analyzed by quantitative real-time RT-PCR. FoxP3 protein expression was assessed by immunohistochemistry. FoxP3 mRNA expression in all infertile patients with EM was significantly higher than the control group (P < 0.05) by non-parametric Mann-Whitney U-test. Further analysis based on the extent of EM revealed that FoxP3 mRNA expression in infertile patients with advanced EM was significantly higher than the mild EM group and the control group (P < 0.05). Immunohistochemistry analysis showed predominant positive staining for FoxP3 protein in the endometrial stroma. In addition, the number of FoxP3+ cells in the eutopic endometrium of infertile women with advanced EM was marginally higher than the mild EM group and the control group, although the differences were not statistically significant (P > 0.05) by two-tailed t-tests. These findings suggest that FoxP3+ Tregs in the peri-implantation endometrium might participate in the pathogenesis of advanced EM. However, they are not directly involved in the pathogenesis of advanced EM associated with infertility. The differential expression of FoxP3 in infertile women with mild EM and advanced EM implicates that notable differences in the uterine immune status are likely involved in the pathogenesis of mild EM associated with infertility in the peri-implantation endometrium.
    Reproductive Biology and Endocrinology 04/2012; 10:34. · 2.41 Impact Factor
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    ABSTRACT: The plant hormone cytokinin plays important roles in various aspects of plant growth and development. Cytokinin signaling is mediated by a multistep phosphorelay similar to bacterial two-component system. Type-B ARRs lie at the end of the cytokinin signaling, typically mediating the output response. However, it is still unclear how type-B ARRs are regulated in response to cytokinin. Typical type-B ARR contains an N-terminal receiver domain and a C-terminal effector domain. In this study, we performed a genome-wild comparative analysis by overexpressing full length and C-terminal effector domain of seven representative type-B ARRs. Our results indicated that overexpression of C-terminal effector domain causes short primary roots and short hypocotyls without the addition of cytokinin, suggesting that the inhibitory role of the receiver domain in the activity of the effector domain is a common mechanism in type-B ARRs. To investigate how the receiver domain inhibits the activity of the effector domain, we performed a deletion analysis. We found that deletion of the initial 45 residues of ARR18 (the 45 residues from N-terminus) causes pleiotropic growth defects by directly inducing cytokinin responsive genes. Together, our results suggest that the initial 45 residues are critical for the inhibitory role of the receiver domain to the effector domain in ARR18.
    Journal of Genetics and Genomics 01/2012; 39(1):37-46. · 2.08 Impact Factor
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    Jian Zhang, Chong Teng, Yan Liang
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    ABSTRACT: Programmed cell death (PCD) plays an important role in plant growth and development as well as in stress responses. During male gametophyte development, it has been proposed that PCD may act as a cellular surveillance mechanism to ensure successful progression of male gametogenesis, and this suicide protective machinery is repressed under favorable growth conditions. However, the regulatory mechanism of male gametophyte-specific PCD remains unknown. Here, we report the use of a TdT-mediated dUTP nick-end labeling-based strategy for genetic screening of Arabidopsis mutants that present PCD phenotype during male gametophyte development. By using this approach, we identified 12 mutants, designated as pcd in male gametogenesis (pig). pig mutants are defective at various stages of male gametophyte development, among which nine pig mutants show a microspore-specific PCD phenotype occurring mainly around pollen mitosis I or the bicellular stage. The PIG1 gene was identified by map-based cloning, and was found to be identical to ATAXIA TELANGIECTASIA MUTATED (ATM), a highly conserved gene in eukaryotes and a key regulator of the DNA damage response. Our results suggest that PCD may act as a general mechanism to safeguard the entire process of male gametophyte development.
    Protein & Cell 10/2011; 2(10):837-44. · 3.22 Impact Factor
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    ABSTRACT: Exposure to mercury causes severe damage to plants, animals and even humans. Concern over mercury toxicity has encouraged the development of efficient, sensitive, and selective methods for the in vivo detection of mercury. Although a variety of studies have been published describing fluorescence imaging of mercury in animal cells and tissues, no in vivo monitoring has been developed for plant systems until now. In this paper, we report the semi-quantitative fluorescence imaging of Hg2+ ions in a common model plant Arabidopsis thaliana (A. thaliana), with rhodamine B thiolactone (RBS) as a novel Hg2+ probe. The experimental results show that RBS is plant cell wall and cell membrane permeable, and the probe responds selectively to Hg2+ ions instead of the other species in plant systems. Real-time monitoring of Hg2+ absorption in roots of A. thaliana by RBS shows that saturation of Hg2+ uptake could occur in a short period of 3 days at most. The transportation and accumulation of Hg2+ ions in roots of A. thaliana have also been studied, revealing that most of Hg2+ ions reside in root cap and meristematic zone, and only a small amount of Hg2+ ions can reach the maturation zone. This indicates that the interaction of Hg2+ ions with any Hg2+-philic species including proteins in these regions may be responsible for plant poisoning and even death.
    Sensors and Actuators B Chemical 03/2011; 153(1):261-265. · 3.84 Impact Factor
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    ABSTRACT: Cytokinin signaling is mediated by a multiple-step phosphorelay. Key components of the phosphorelay consist of the histidine kinase (HK)-type receptors, histidine phosphotransfer proteins (HP), and response regulators (RRs). Whereas overexpression of a nonreceptor-type HK gene CYTOKININ-INDEPENDENT1 (CKI1) activates cytokinin signaling by an unknown mechanism, mutations in CKI1 cause female gametophytic lethality. However, the function of CKI1 in cytokinin signaling remains unclear. Here, we characterize a mutant allele, cki1-8, that can be transmitted through female gametophytes with low frequency (approximately 0.17%). We have recovered viable homozygous cki1-8 mutant plants that grow larger than wild-type plants, show defective megagametogenesis and rarely set enlarged seeds. We found that CKI1 acts upstream of AHP (Arabidopsis HP) genes, independently of cytokinin receptor genes. Consistently, an ahp1,2-2,3,4,5 quintuple mutant, which contains an ahp2-2 null mutant allele, exhibits severe defects in megagametogenesis, with a transmission efficiency of <3.45% through female gametophytes. Rarely recovered ahp1,2-2,3,4,5 quintuple mutants are seedling lethal. Finally, the female gametophytic lethal phenotype of cki1-5 (a null mutant) can be partially rescued by IPT8 or ARR1 (a type-B Arabidopsis RR) driven by a CKI1 promoter. These results define a genetic pathway consisting of CKI1, AHPs, and type-B ARRs in the regulation of female gametophyte development and vegetative growth.
    The Plant Cell 04/2010; 22(4):1232-48. · 9.25 Impact Factor
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    ABSTRACT: Metabolism of S-nitrosoglutathione (GSNO), a major biologically active nitric oxide (NO) species, is catalyzed by the evolutionally conserved GSNO reductase (GSNOR). Previous studies showed that the Arabidopsis GSNOR1/HOT5 gene regulates salicylic acid signaling and thermotolerance by modulating the intracellular S-nitrosothiol level. Here, we report the characterization of the Arabidopsis paraquat resistant2-1 (par2-1) mutant that shows an anti-cell death phenotype. The production of superoxide in par2-1 is comparable to that of wild-type plants when treated by paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride), suggesting that PAR2 acts downstream of superoxide to regulate cell death. PAR2, identified by positional cloning, is shown to be identical to GSNOR1/HOT5. The par2-1 mutant carries a missense mutation in a highly conserved glycine, which renders the mutant protein unstable. Compared to wild type, par2-1 mutant has a higher NO level, as revealed by staining with 4,5-diaminofluorescein diacetate. Consistent with this result, wild-type plants treated with an NO donor display resistance to paraquat. Interestingly, the GSNOR1/HOT5/PAR2 protein level, other than its steady-state mRNA level, is induced by paraquat, but is reduced by NO donors. Taken together, these results suggest that GSNOR1/HOT5/PAR2 plays an important role in regulating cell death in plant cells through modulating intracellular NO level.
    Cell Research 10/2009; 19(12):1377-87. · 10.53 Impact Factor
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    ABSTRACT: Cytokinin is a critical growth regulator for various aspects of plant growth and development. In Arabidopsis, cytokinin signaling is mediated by a two-component system-based phosphorelay that transmits a signal from the receptors, through histidine phosphotransfer proteins, to the downstream response regulators (ARRs). Of these ARRs, type-A ARR genes, whose transcription can be rapidly induced by cytokinin, act as negative regulators of cytokinin signaling. However, because of functional redundancy, the function of type-A ARR genes in plant growth and development is not well understood by analyzing loss-of-function mutants. In this study, we performed a comparative functional study on all ten type-A ARR genes by analyzing transgenic plants overexpressing these ARR genes fused to a MYC epitope tag. Overexpression of ARR genes results in a variety of cytokinin-associated phenotypes. Notably, overexpression of different ARR transgenes causes diverse phenotypes, even between phylogenetically closely-related gene pairs, such as within the ARR3-ARR4 and ARR5-ARR6 pairs. We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation. Moreover, similar to that of previously characterized ARR5, ARR6 and ARR7, stability of ARR16 and ARR17, possibly including ARR8 and ARR15, is regulated by cytokinin. These results suggest that type-A ARR proteins are regulated by a combinatorial mechanism involving both the cytokinin and proteasome pathways, thereby executing distinctive functions in plant growth and development.
    Cell Research 08/2009; 19(10):1178-90. · 10.53 Impact Factor
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    ABSTRACT: In plants, fatty acids are de novo synthesized predominantly in plastids from acetyl-coenzyme A. Although fatty acid biosynthesis has been biochemically well studied, little is known about the regulatory mechanisms of the pathway. Here, we show that overexpression of the Arabidopsis (Arabidopsis thaliana) LEAFY COTYLEDON1 (LEC1) gene causes globally increased expression of fatty acid biosynthetic genes, which are involved in key reactions of condensation, chain elongation, and desaturation of fatty acid biosynthesis. In the plastidial fatty acid synthetic pathway, over 58% of known enzyme-coding genes are up-regulated in LEC1-overexpressing transgenic plants, including those encoding three subunits of acetyl-coenzyme A carboxylase, a key enzyme controlling the fatty acid biosynthesis flux. Moreover, genes involved in glycolysis and lipid accumulation are also up-regulated. Consistent with these results, levels of major fatty acid species and lipids were substantially increased in the transgenic plants. Genetic analysis indicates that the LEC1 function is partially dependent on ABSCISIC ACID INSENSITIVE3, FUSCA3, and WRINKLED1 in the regulation of fatty acid biosynthesis. Moreover, a similar phenotype was observed in transgenic Arabidopsis plants overexpressing two LEC1-like genes of Brassica napus. These results suggest that LEC1 and LEC1-like genes act as key regulators to coordinate the expression of fatty acid biosynthetic genes, thereby representing promising targets for genetic improvement of oil production plants.
    Plant physiology 09/2008; 148(2):1042-54. · 6.56 Impact Factor
  • Yan Liang, JianRu Zuo, WeiCai Yang
    Chinese Science Bulletin 06/2007; 52(13):1729-1733. · 1.37 Impact Factor

Publication Stats

199 Citations
62.45 Total Impact Points


  • 2012
    • Shanghai University
      Shanghai, Shanghai Shi, China
  • 2011–2012
    • Chinese Academy of Sciences
      • Institute of Genetics and Developmental Biology
      Peping, Beijing, China
  • 2008–2012
    • Northeast Institute of Geography and Agroecology
      • • Institute of Genetics and Developmental Biology
      • • State Key Laboratory of Plant Genomics
      Beijing, Beijing Shi, China