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CRISPR/Cas9介导的[基因名称]破坏导致金鱼()的正中鳍发育异常和体节发生异常。 (注:原文中“Leads to Abnormal Median Fin Development and Somitogenesis in Goldfish ()”括号内应有具体基因名称等关键信息缺失未完整给出)

CRISPR/Cas9-Mediated Disruption of Leads to Abnormal Median Fin Development and Somitogenesis in Goldfish ().

作者信息

Li Huijuan, Zhang Rong, Wang Xiaowen, Liu Lili, Yao Zhigang, Zhu Hua

机构信息

Beijing Key Laboratory of Fishery Biotechnology, Fisheries Science Institute, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China.

出版信息

Int J Mol Sci. 2025 Jul 22;26(15):7067. doi: 10.3390/ijms26157067.


DOI:10.3390/ijms26157067
PMID:40806200
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12345836/
Abstract

In this study, we demonstrated that , a co-receptor in the Wnt signaling pathway, is essential for proper median fin formation and somitogenesis in goldfish. We analyzed the gene's sequence features and expression patterns in both wen-type and egg-type goldfish, uncovering distinct tissue-specific expression differences between the two varieties. To explore the functional role of , we performed CRISPR/Cas9-mediated gene knockout using eight designed single-guide RNAs (sgRNAs), of which four showed effective targeting. Three high-efficiency sgRNAs were selected and co-injected into embryos to achieve complete gene disruption. Morphological assessments and X-ray microtomography (μCT) imaging of the resulting mutants revealed various abnormalities, including defects in the dorsal, caudal, and anal fins, as well as skeletal deformities near the caudal peduncle. These results confirm that plays a key role in median fin development and axial patterning, offering new insights into the genetic regulation of fin formation in teleost fish.

摘要

在本研究中,我们证明了Wnt信号通路中的共受体 在金鱼的正中鳍形成和体节发生过程中至关重要。我们分析了该基因在文种金鱼和蛋种金鱼中的序列特征和表达模式,发现这两个品种之间存在明显的组织特异性表达差异。为了探究 的功能作用,我们使用八个设计好的单向导RNA(sgRNA)进行了CRISPR/Cas9介导的基因敲除,其中四个显示出有效的靶向作用。选择了三个高效sgRNA并共同注射到胚胎中以实现完全的基因破坏。对所得突变体的形态学评估和X射线显微断层扫描(μCT)成像揭示了各种异常情况,包括背鳍、尾鳍和臀鳍的缺陷,以及尾柄附近的骨骼畸形。这些结果证实了 在正中鳍发育和轴向模式形成中起关键作用,为硬骨鱼鳍形成的遗传调控提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/7bc12c547fd5/ijms-26-07067-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/4a97a55ad2b7/ijms-26-07067-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/f51a741caddb/ijms-26-07067-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/7f0ecfca0be1/ijms-26-07067-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/d72343f32261/ijms-26-07067-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/23b6813e1e2f/ijms-26-07067-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/88abd1d93d92/ijms-26-07067-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/5811fdcee147/ijms-26-07067-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/3e7bbe607987/ijms-26-07067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/cf5be28e8d6a/ijms-26-07067-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/9020abceb773/ijms-26-07067-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/7bc12c547fd5/ijms-26-07067-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/4a97a55ad2b7/ijms-26-07067-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/f51a741caddb/ijms-26-07067-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/7f0ecfca0be1/ijms-26-07067-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/d72343f32261/ijms-26-07067-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/23b6813e1e2f/ijms-26-07067-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/88abd1d93d92/ijms-26-07067-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/5811fdcee147/ijms-26-07067-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/3e7bbe607987/ijms-26-07067-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/cf5be28e8d6a/ijms-26-07067-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/9020abceb773/ijms-26-07067-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dff0/12345836/7bc12c547fd5/ijms-26-07067-g011.jpg

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CRISPR/Cas9-Mediated Disruption of Leads to Abnormal Median Fin Development and Somitogenesis in Goldfish ().

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本文引用的文献

[1]
Enhancing genome editing efficiency in goldfish (Carassius auratus) through utilization of CRISPR-Cas12a (Cpf1) temperature dependency.

Int J Biol Macromol. 2025-5

[2]
Teleost code defines regional identities competent for the formation of dorsal and anal fins.

Proc Natl Acad Sci U S A. 2024-6-18

[3]
The USP46 complex deubiquitylates LRP6 to promote Wnt/β-catenin signaling.

Nat Commun. 2023-10-5

[4]
Structure of the Wnt-Frizzled-LRP6 initiation complex reveals the basis for coreceptor discrimination.

Proc Natl Acad Sci U S A. 2023-3-14

[5]
Disruption of T-box transcription factor eomesa results in abnormal development of median fins in Oujiang color common carp Cyprinus carpio.

PLoS One. 2023

[6]
Zebrafish mutants reveal unexpected role of Lrp5 in osteoclast regulation.

Front Endocrinol (Lausanne). 2022

[7]
Developmental independence of median fins from the larval fin fold revises their evolutionary origin.

Sci Rep. 2022-5-7

[8]
An Fgf-Shh positive feedback loop drives growth in developing unpaired fins.

Proc Natl Acad Sci U S A. 2022-3-8

[9]
Genotype affects Individual Susceptibility to Nonalcoholic Fatty Liver Disease and Silibinin Therapeutic Response via Wnt/β-catenin-Cyp2e1 Signaling.

Int J Biol Sci. 2021

[10]
The bowfin genome illuminates the developmental evolution of ray-finned fishes.

Nat Genet. 2021-9

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