|
Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish
Chao Liu,Weirui Ma,Wenjing Su and Jian Zhang
Development
Abstract
The precise formation of three-dimensional motor circuits is essential for movement control. Within these circuits, motoneurons (MNs) are specified from spinal progenitors by dorsoventral signals and distinct transcriptional programs. Different MN subpopulations have stereotypic cell body positions and show specific spatial axon trajectories. Our knowledge of MN axon outgrowth remains incomplete. Here, we report a zebrafish gene-trap mutant, short lightning (slg), in which prdm14expression is disrupted. slg mutant embryos show shortened axons in caudal primary (CaP) MNs resulting in defective embryonic movement. Both the CaP neuronal defects and behavior abnormality of the mutants can be phenocopied by injection of a prdm14morpholino into wild-type embryos. By removing a copy of the inserted transposon from homozygous mutants, prdm14expression and normal embryonic movement were restored, confirming that loss of prdm14expression accounts for the observed defects. Mechanistically, prdm14protein binds to the promoter region of islet2, a known transcription factor required for CaP development. Notably, disruption of islet2 function caused similar CaP axon outgrowth defects as observed in slg mutant embryos. Furthermore, overexpression of islet2 in slg mutant embryos rescued the shortened CaP axon phenotypes. Together, these data reveal that prdm14regulates CaP axon outgrowth through activation of islet2 expression.
|
论文编号: |
DOI:10.1242/dev.083055 |
论文题目: |
Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish |
英文论文题目: |
Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish |
第一作者: |
Chao Liu,Weirui Ma,Wenjing Su and Jian Zhang |
英文第一作者: |
Chao Liu,Weirui Ma,Wenjing Su and Jian Zhang |
联系作者: |
|
英文联系作者: |
|
外单位作者单位: |
|
英文外单位作者单位: |
|
发表年度: |
2012-11-11 |
卷: |
|
期: |
|
页码: |
|
摘要: |
The precise formation of three-dimensional motor circuits is essential for movement control. Within these circuits, motoneurons (MNs) are specified from spinal progenitors by dorsoventral signals and distinct transcriptional programs. Different MN subpopulations have stereotypic cell body positions and show specific spatial axon trajectories. Our knowledge of MN axon outgrowth remains incomplete. Here, we report a zebrafish gene-trap mutant, short lightning (slg), in which prdm14expression is disrupted. slg mutant embryos show shortened axons in caudal primary (CaP) MNs resulting in defective embryonic movement. Both the CaP neuronal defects and behavior abnormality of the mutants can be phenocopied by injection of a prdm14morpholino into wild-type embryos. By removing a copy of the inserted transposon from homozygous mutants, prdm14expression and normal embryonic movement were restored, confirming that loss of prdm14expression accounts for the observed defects. Mechanistically, prdm14protein binds to the promoter region of islet2, a known transcription factor required for CaP development. Notably, disruption of islet2 function caused similar CaP axon outgrowth defects as observed in slg mutant embryos. Furthermore, overexpression of islet2 in slg mutant embryos rescued the shortened CaP axon phenotypes. Together, these data reveal that prdm14regulates CaP axon outgrowth through activation of islet2 expression. |
英文摘要: |
The precise formation of three-dimensional motor circuits is essential for movement control. Within these circuits, motoneurons (MNs) are specified from spinal progenitors by dorsoventral signals and distinct transcriptional programs. Different MN subpopulations have stereotypic cell body positions and show specific spatial axon trajectories. Our knowledge of MN axon outgrowth remains incomplete. Here, we report a zebrafish gene-trap mutant, short lightning (slg), in which prdm14expression is disrupted. slg mutant embryos show shortened axons in caudal primary (CaP) MNs resulting in defective embryonic movement. Both the CaP neuronal defects and behavior abnormality of the mutants can be phenocopied by injection of a prdm14morpholino into wild-type embryos. By removing a copy of the inserted transposon from homozygous mutants, prdm14expression and normal embryonic movement were restored, confirming that loss of prdm14expression accounts for the observed defects. Mechanistically, prdm14protein binds to the promoter region of islet2, a known transcription factor required for CaP development. Notably, disruption of islet2 function caused similar CaP axon outgrowth defects as observed in slg mutant embryos. Furthermore, overexpression of islet2 in slg mutant embryos rescued the shortened CaP axon phenotypes. Together, these data reveal that prdm14regulates CaP axon outgrowth through activation of islet2 expression. |
刊物名称: |
Development |
英文刊物名称: |
Development |
论文全文: |
|
英文论文全文: |
|
全文链接: |
|
其它备注: |
Chao Liu,Weirui Ma,Wenjing Su and Jian Zhang. Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish. Development. DOI:10.1242/dev.083055 |
英文其它备注: |
|
学科: |
|
英文学科: |
|
影响因子: |
|
第一作者所在部门: |
|
英文第一作者所在部门: |
|
论文出处: |
|
英文论文出处: |
|
论文类别: |
|
英文论文类别: |
|
参与作者: |
|
英文参与作者: |
|
|