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Start Over Author "Li, Donghao" Publisher elsevier b.v.
147 results on '"Li, Donghao"'

49. TMK4-mediated FIP37 phosphorylation regulates auxin-triggered N6-methyladenosine modification of auxin biosynthetic genes in Arabidopsis.

Author

Li, Bin, Zhou, Qiting, Cai, Linjun, Li, Lan, Xie, Chong, Li, Donghao, Zhu, Fan, Li, Xiushan, Zhao, Xiaoying, Liu, Xuanming, Shen, Lisha, Xu, Tongda, and He, Chongsheng

Abstract

The dynamics of N 6 -methyladenosine (m6A) mRNA modification are tightly controlled by the m6A methyltransferase complex and demethylases. Here, we find that auxin treatment alters m6A modification on auxin-responsive genes. Mechanically, TRANSMEMBRANE KINASE 4 (TMK4), a component of the auxin signaling pathway, interacts with and phosphorylates FKBP12-INTERACTING PROTEIN 37 (FIP37), a core component of the m6A methyltransferase complex, in an auxin-dependent manner. Phosphorylation of FIP37 enhances its interaction with RNA, thereby increasing m6A modification on its target genes, such as NITRILASE 1 (NIT1), a gene involved in indole-3-acetic acid (IAA) biosynthesis. 1-Naphthalacetic acid (NAA) treatment accelerates the mRNA decay of NIT1 , in a TMK4- and FIP37-dependent manner, which leads to inhibition of auxin biosynthesis. Our findings identify a regulatory mechanism by which auxin modulates m6A modification through the phosphorylation of FIP37, ultimately affecting mRNA stability and auxin biosynthesis in plants. [Display omitted] • Auxin induces alterations in m6A modification • TMK4 interacts and phosphorylates FIP37 in an auxin-dependent manner • Auxin treatment accelerates the mRNA decay rate of NIT1 Li et al. show that auxin-induced m6A modification alterations driven by the TMK4-FIP37 axis have an impact on gene expression and auxin biosynthesis. This study offers insights into the dynamic interplay between RNA modification and hormone signaling in plants. [ABSTRACT FROM AUTHOR]

Published
2024
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50. DCT based multi-head attention-BiGRU model for EEG source location.

Author

Zhang, Boyuan, Li, Donghao, and Wang, Dongqing

Subjects
DISCRETE cosine transforms, ELECTROENCEPHALOGRAPHY, MAGNETOENCEPHALOGRAPHY, INVERSE problems, SIGNAL-to-noise ratio
Abstract

• Multi-head attention captures the relationships among distinct features within the EEG signals. • DCT on brain signals is performed, its coefficients of low frequencies are retained. • BiGRUs map the relationship between recorded EEG signals and truncated DCT coefficients. • The BiGRU number is reduced with truncated DCT coefficients as outputs. • Comparison experiments verify that the proposed MA-DCT-BiGRU configuration is effective. Electroencephalogram source imaging (ESI) pertains to localize brain sources. Due to the one-to-many relationship between electroencephalogram (EEG) signals and brain sources, ESI becomes a complex inverse problem with poor conditioning, leaving a lot of research space. This article proposes an enhanced multi-head attention (MA) and discrete cosine transform (DCT) based Bidirectional Gated Recurrent Unit (BiGRU) (MA-DCT-BiGRU for short) for addressing the EEG inverse problem. Initially, EEG signal characteristics are captured employing multi-head attention with the inclusion of average hidden states. Then, the DCT is used to project brain source signals into the low, medium, and high frequency subspaces composed of spatial frequency basis vectors. The spatial low-frequency component serves as a filter for extended source reconstruction. Subsequently, BiGRU is employed to learn the mapping from the output of the attention layer to the low frequency DCT coefficients of the brain-derived signals. The simulation results undeniably establish the superiority of the MA-DCT-BiGRU configuration in comparison to other state-of-the-art (SOA) methods for source recovery, irrespective of the source modes and signal-to-noise ratio conditions. Experimental results, utilizing both synthetic and actual epilepsy data, clearly demonstrate the effectiveness of the framework presented in this article for epileptogenic area localization. [ABSTRACT FROM AUTHOR]

Published
2024
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