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花粉管 homogalacturonan 合成受阻可缓解拟南芥 O-岩藻糖基转移酶 1 突变体中的花粉管穿透缺陷。

Disruption of pollen tube homogalacturonan synthesis relieves pollen tube penetration defects in the Arabidopsis O-FUCOSYLTRANSFERASE1 mutant.

机构信息

Department of Biochemistry and Molecular Biology, University of Nevada, Reno, 1664 N. Virginia St. MS0330, Reno, NV, 89557, USA.

出版信息

Plant Reprod. 2023 Sep;36(3):263-272. doi: 10.1007/s00497-023-00468-5. Epub 2023 May 24.

Abstract

During angiosperm sexual reproduction, pollen tubes must penetrate through multiple cell types in the pistil to mediate successful fertilization. Although this process is highly choreographed and requires complex chemical and mechanical signaling to guide the pollen tube to its destination, aspects of our understanding of pollen tube penetration through the pistil are incomplete. Our previous work demonstrated that disruption of the Arabidopsis thaliana O-FUCOSYLTRANSFERASE1 (OFT1) gene resulted in decreased pollen tube penetration through the stigma-style interface. Here, we demonstrate that second site mutations of Arabidopsis GALACTURONOSYLTRANSFERASE 14 (GAUT14) effectively suppress the phenotype of oft1 mutants, partially restoring silique length, seed set, pollen transmission, and pollen tube penetration deficiencies in navigating the female reproductive tract. These results suggest that disruption of pectic homogalacturonan (HG) synthesis can alleviate the penetrative defects associated with the oft1 mutant and may implicate pectic HG deposition in the process of pollen tube penetration through the stigma-style interface in Arabidopsis. These results also support a model in which OFT1 function directly or indirectly modifies structural features associated with the cell wall, with the loss of oft1 leading to an imbalance in the wall composition that can be compensated for by a reduction in pectic HG deposition.

摘要

在被子植物有性生殖过程中,花粉管必须穿透雌蕊中的多种细胞类型才能介导成功受精。虽然这个过程高度协调,并需要复杂的化学和机械信号来引导花粉管到达目的地,但我们对花粉管穿透雌蕊的理解还不完全。我们之前的工作表明,拟南芥 O-岩藻糖基转移酶 1(OFT1)基因的破坏导致花粉管穿透柱头-花柱界面的能力下降。在这里,我们证明拟南芥半乳糖基转移酶 14(GAUT14)的第二点突变有效地抑制了 oft1 突变体的表型,部分恢复了长角果长度、结实率、花粉传递和花粉管穿透能力的缺陷,从而在雌性生殖道中导航。这些结果表明,果胶同型半乳糖醛酸聚糖(HG)合成的破坏可以减轻 oft1 突变体相关的穿透缺陷,并可能暗示果胶 HG 的沉积参与了花粉管穿透拟南芥柱头-花柱界面的过程。这些结果还支持了这样一种模型,即 OFT1 功能直接或间接修饰与细胞壁相关的结构特征,oft1 的缺失导致细胞壁组成失衡,这种失衡可以通过减少果胶 HG 的沉积来补偿。

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