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细胞分裂素通过破坏 PIN3a 介导的生长素在胚珠表皮中的不对称积累来抑制棉花纤维起始。

Cytokinin inhibits cotton fiber initiation by disrupting PIN3a-mediated asymmetric accumulation of auxin in the ovule epidermis.

机构信息

Biotechnology Research Center, Southwest University, Beibei, Chongqing, P. R. China.

出版信息

J Exp Bot. 2019 Jun 28;70(12):3139-3151. doi: 10.1093/jxb/erz162.

DOI:10.1093/jxb/erz162
PMID:30970146
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6598071/
Abstract

Auxin-dependent cell expansion is crucial for initiation of fiber cells in cotton (Gossypium hirsutum), which ultimately determines fiber yield and quality. However, the regulation of this process is far from being well understood. In this study, we demonstrate an antagonistic effect between cytokinin (CK) and auxin on cotton fiber initiation. In vitro and in planta experiments indicate that enhanced CK levels can reduce auxin accumulation in the ovule integument, which may account for the defects in the fiberless mutant xu142fl. In turn, supplementation with auxin can recover fiber growth of CK-treated ovules and mutant ovules. We further found that GhPIN3a is a key auxin transporter for fiber-cell initiation and is polarly localized to the plasma membranes of non-fiber cells, but not to those of fiber cells. This polar localization allows auxin to be transported within the ovule integument while specifically accumulating in fiber cells. We show that CKs antagonize the promotive effect of auxin on fiber cell initiation by undermining asymmetric accumulation of auxin in the ovule epidermis through down-regulation of GhPIN3a and disturbance of the polar localization of the protein.

摘要

生长素依赖性细胞扩张对于棉花(Gossypium hirsutum)纤维细胞的起始至关重要,这最终决定了纤维的产量和质量。然而,这一过程的调节机制远未被充分理解。在本研究中,我们证明了细胞分裂素(CK)和生长素对棉花纤维起始的拮抗作用。体外和体内实验表明,增强的 CK 水平可以减少珠被中生长素的积累,这可能是无纤维突变体 xu142fl 缺陷的原因。相反,生长素的补充可以恢复 CK 处理的胚珠和突变体胚珠的纤维生长。我们进一步发现,GhPIN3a 是纤维细胞起始的关键生长素转运蛋白,它在珠被的质膜上呈极性定位,但不在纤维细胞的质膜上。这种极性定位允许生长素在珠被内运输,同时特异性地在纤维细胞中积累。我们表明,CK 通过下调 GhPIN3a 和扰乱蛋白的极性定位,破坏生长素在珠被表皮中的不对称积累,从而拮抗生长素对纤维细胞起始的促进作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/a43e824f6e57/erz162f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/735bc5892efa/erz162f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/4d16357ca506/erz162f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/a1a4183b4ca5/erz162f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/74fa974d557d/erz162f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/c2c1fb06207d/erz162f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/ac3fecc36fc9/erz162f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/a43e824f6e57/erz162f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/735bc5892efa/erz162f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/4d16357ca506/erz162f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/a1a4183b4ca5/erz162f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/74fa974d557d/erz162f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/c2c1fb06207d/erz162f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/ac3fecc36fc9/erz162f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f27/6598071/a43e824f6e57/erz162f0007.jpg

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