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MADS盒基因XAANTAL1通过直接调控过氧化物酶28和视网膜母细胞瘤相关基因,参与拟南芥主根生长和柱干细胞模式以响应活性氧。

The MADS-box gene XAANTAL1 participates in Arabidopsis thaliana primary root growth and columella stem cell patterns in response to ROS, via direct regulation of PEROXIDASE 28 and RETINOBLASTOMA-RELATED genes.

作者信息

Zluhan-Martínez Estephania, Castañón-Suárez Claudio A, Gutiérrez-Rodríguez Mario A, Lledías Fernando, Zhang Tao, Peng Jesús T, Dickinson Jazz, Sánchez Rodríguez Diana Belén, Sánchez María de la Paz, García-Ponce Berenice, Álvarez-Buylla Elena R, Garay-Arroyo Adriana

机构信息

Laboratorio de Genética Molecular, Desarrollo y Evolución de Plantas, Departamento de Ecología Funcional, Instituto de Ecología, Universidad Nacional Autónoma de México, Ciudad de México, CP 04510, México.

Posgrado en Ciencias Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, CP 04510, México.

出版信息

J Exp Bot. 2025 Jan 10;76(2):411-432. doi: 10.1093/jxb/erae415.

DOI:10.1093/jxb/erae415
PMID:39377268
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11714753/
Abstract

The balance between cell growth, proliferation, and differentiation emerges from gene regulatory networks coupled to various signal transduction pathways, including reactive oxygen species (ROS) and transcription factors (TFs), enabling developmental responses to environmental cues. The primary root of Arabidopsis thaliana has become a valuable system for unravelling such networks. Recently, the role of TFs that mediate ROS inhibition of primary root growth has begun to be characterized. This study demonstrates that the MADS-box TF gene XAANTAL1 (XAL1) is an essential regulator of hydrogen peroxide (H2O2) in primary root growth and root stem cell niche identity. Interestingly, our findings indicated that XAL1 acts as a positive regulator of H2O2 concentration in the root meristem by directly regulating genes involved in oxidative stress response, such as PEROXIDASE 28 (PER28). Moreover, we found that XAL1 is necessary for the H2O2-induced inhibition of primary root growth through the negative regulation of peroxidase and catalase activities. Furthermore, XAL1, in conjunction with RETINOBLASTOMA-RELATED (RBR), is essential for positively regulating the differentiation of columella stem cells and for participating in primary root growth inhibition in response to oxidative stress induced by H2O2 treatment.

摘要

细胞生长、增殖和分化之间的平衡源于与各种信号转导途径(包括活性氧(ROS)和转录因子(TFs))耦合的基因调控网络,从而实现对环境线索的发育响应。拟南芥的主根已成为揭示此类网络的重要系统。最近,介导ROS对主根生长抑制作用的TFs的作用已开始得到表征。本研究表明,MADS盒TF基因XAANTAL1(XAL1)是过氧化氢(H2O2)在主根生长和根干细胞龛身份中的关键调节因子。有趣的是,我们的研究结果表明,XAL1通过直接调节参与氧化应激反应的基因(如过氧化物酶28(PER28)),作为根分生组织中H2O2浓度的正调节因子。此外,我们发现XAL1通过对过氧化物酶和过氧化氢酶活性的负调节,对于H2O2诱导的主根生长抑制是必需的。此外,XAL1与视网膜母细胞瘤相关蛋白(RBR)一起,对于正向调节柱干细胞的分化以及参与响应H2O2处理诱导的氧化应激的主根生长抑制至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/fd8cec21c799/erae415_fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/d71aa87a4650/erae415_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/b3a126ec92fa/erae415_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/4c9026a6fe75/erae415_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/c403c9f0ec1b/erae415_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/8fbd7a11a6b3/erae415_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/b8c76f76e5bc/erae415_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/a0431265bd25/erae415_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/726f718436ee/erae415_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/89e4fb64aa0d/erae415_fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/fd8cec21c799/erae415_fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/d71aa87a4650/erae415_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/b3a126ec92fa/erae415_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/4c9026a6fe75/erae415_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/c403c9f0ec1b/erae415_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/8fbd7a11a6b3/erae415_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/b8c76f76e5bc/erae415_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/a0431265bd25/erae415_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/726f718436ee/erae415_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/89e4fb64aa0d/erae415_fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a84/11714753/fd8cec21c799/erae415_fig10.jpg

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