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Qingshun Zhao - One of the best experts on this subject based on the ideXlab platform.
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zebrafish microrna mir 210 5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mrnas downstream of gata4 5 6 transcription factor genes
Journal of Biological Chemistry, 2019Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua Yao, Qingshun ZhaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis
Developmental Dynamics, 2014Co-Authors: Xiaohua Dong, Dong Liang, Qingshun ZhaoAbstract:Background: Although Ncor1 and Ncor2, the co-repressors that can actively repress gene transcription through binding nuclear receptors in the absence of ligands, are crucial to vertebrate embryogenesis, their roles in its primitive Myelopoiesis remain unknown. We investigated the function of ncor1 or ncor2 in zebrafish embryos by antisense morpholino knocking down technologies. Results: Development of both mfap4+ macrophages and mpx+ neutrophils was abolished in ncor2 morphants, whereas development of mpx+ neutrophils was depleted in ncor1 morphants. ncor2 was essential to the development of spi1b+ myeloid precursors but not anterior hemangioblasts whereas ncor1 was dispensable to the specification of spi1b+ myeloid precursors and anterior hemangioblasts. Overexpressing spi1b could partially rescue expressions of mfap4 and mpx in ncor2 morphants. Furthermore, overexpressing tal1/lmo2 could well rescue the defective Myelopoiesis in both ncor1 and ncor2 morphants. Conclusions: Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis. ncor2 could parallel with tal1/lmo2 and acted upstream of spi1b to produce mature macrophages and neutrophils during primitive Myelopoiesis. The role of ncor1 in zebrafish Myelopoiesis could be substituted by excessive Tal1/Lmo2. Developmental Dynamics 243:1544–1553, 2014. © 2014 Wiley Periodicals, Inc.
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Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2013Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increase
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Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2012Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increases aldh1a2 expression. The results reveal that RA signaling acts downstream of gata4/5/6 to control primitive Myelopoiesis. But, 4-diethylamino-benzaldehyde fails to rescue the defective primitive Myelopoiesis in either cloche embryos or lycat morphants. Taken together, our results demonstrate that RA signaling restricts zebrafish primitive Myelopoiesis through acting downstream of gata4/5/6, upstream of, or parallel to, cloche, and upstream of scl.
Xiaohua Dong - One of the best experts on this subject based on the ideXlab platform.
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zebrafish microrna mir 210 5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mrnas downstream of gata4 5 6 transcription factor genes
Journal of Biological Chemistry, 2019Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua Yao, Qingshun ZhaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Zebrafish microRNA miR-210-5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mRNAs downstream of gata4/5/6 transcription factor genes
Journal of Biological Chemistry, 2018Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua YaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis
Developmental Dynamics, 2014Co-Authors: Xiaohua Dong, Dong Liang, Qingshun ZhaoAbstract:Background: Although Ncor1 and Ncor2, the co-repressors that can actively repress gene transcription through binding nuclear receptors in the absence of ligands, are crucial to vertebrate embryogenesis, their roles in its primitive Myelopoiesis remain unknown. We investigated the function of ncor1 or ncor2 in zebrafish embryos by antisense morpholino knocking down technologies. Results: Development of both mfap4+ macrophages and mpx+ neutrophils was abolished in ncor2 morphants, whereas development of mpx+ neutrophils was depleted in ncor1 morphants. ncor2 was essential to the development of spi1b+ myeloid precursors but not anterior hemangioblasts whereas ncor1 was dispensable to the specification of spi1b+ myeloid precursors and anterior hemangioblasts. Overexpressing spi1b could partially rescue expressions of mfap4 and mpx in ncor2 morphants. Furthermore, overexpressing tal1/lmo2 could well rescue the defective Myelopoiesis in both ncor1 and ncor2 morphants. Conclusions: Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis. ncor2 could parallel with tal1/lmo2 and acted upstream of spi1b to produce mature macrophages and neutrophils during primitive Myelopoiesis. The role of ncor1 in zebrafish Myelopoiesis could be substituted by excessive Tal1/Lmo2. Developmental Dynamics 243:1544–1553, 2014. © 2014 Wiley Periodicals, Inc.
Wenshuang Jia - One of the best experts on this subject based on the ideXlab platform.
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zebrafish microrna mir 210 5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mrnas downstream of gata4 5 6 transcription factor genes
Journal of Biological Chemistry, 2019Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua Yao, Qingshun ZhaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Zebrafish microRNA miR-210-5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mRNAs downstream of gata4/5/6 transcription factor genes
Journal of Biological Chemistry, 2018Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua YaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2013Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increase
-
Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2012Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increases aldh1a2 expression. The results reveal that RA signaling acts downstream of gata4/5/6 to control primitive Myelopoiesis. But, 4-diethylamino-benzaldehyde fails to rescue the defective primitive Myelopoiesis in either cloche embryos or lycat morphants. Taken together, our results demonstrate that RA signaling restricts zebrafish primitive Myelopoiesis through acting downstream of gata4/5/6, upstream of, or parallel to, cloche, and upstream of scl.
Dong Liang - One of the best experts on this subject based on the ideXlab platform.
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zebrafish microrna mir 210 5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mrnas downstream of gata4 5 6 transcription factor genes
Journal of Biological Chemistry, 2019Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua Yao, Qingshun ZhaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Zebrafish microRNA miR-210-5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mRNAs downstream of gata4/5/6 transcription factor genes
Journal of Biological Chemistry, 2018Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua YaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis
Developmental Dynamics, 2014Co-Authors: Xiaohua Dong, Dong Liang, Qingshun ZhaoAbstract:Background: Although Ncor1 and Ncor2, the co-repressors that can actively repress gene transcription through binding nuclear receptors in the absence of ligands, are crucial to vertebrate embryogenesis, their roles in its primitive Myelopoiesis remain unknown. We investigated the function of ncor1 or ncor2 in zebrafish embryos by antisense morpholino knocking down technologies. Results: Development of both mfap4+ macrophages and mpx+ neutrophils was abolished in ncor2 morphants, whereas development of mpx+ neutrophils was depleted in ncor1 morphants. ncor2 was essential to the development of spi1b+ myeloid precursors but not anterior hemangioblasts whereas ncor1 was dispensable to the specification of spi1b+ myeloid precursors and anterior hemangioblasts. Overexpressing spi1b could partially rescue expressions of mfap4 and mpx in ncor2 morphants. Furthermore, overexpressing tal1/lmo2 could well rescue the defective Myelopoiesis in both ncor1 and ncor2 morphants. Conclusions: Ncor1 and Ncor2 play essential but distinct roles in zebrafish primitive Myelopoiesis. ncor2 could parallel with tal1/lmo2 and acted upstream of spi1b to produce mature macrophages and neutrophils during primitive Myelopoiesis. The role of ncor1 in zebrafish Myelopoiesis could be substituted by excessive Tal1/Lmo2. Developmental Dynamics 243:1544–1553, 2014. © 2014 Wiley Periodicals, Inc.
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Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2013Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increase
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Retinoic Acid Signaling Plays a Restrictive Role in Zebrafish Primitive Myelopoiesis
2012Co-Authors: Dong Liang, Wenshuang Jia, Qingshun ZhaoAbstract:Retinoic acid (RA) is known to regulate definitive Myelopoiesis but its role in vertebrate primitive Myelopoiesis remains unclear. Here we report that zebrafish primitive Myelopoiesis is restricted by RA in a dose dependent manner mainly before 11 hpf (hours post fertilization) when anterior hemangioblasts are initiated to form. RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. The result indicates that RA restricts primitive Myelopoiesis by suppressing formation of anterior hemangioblasts. Analyses of ALPM formation suggest that the defective primitive Myelopoiesis resulting from RA treatment before late gastrulation may be secondary to global loss of cells for ALPM fate whereas the developmental defect resulting from RA treatment during 10–11 hpf should be due to ALPM patterning shift. Overexpressions of scl and lmo2 partially rescue the block of primitive Myelopoiesis in the embryos treated with 250 nM RA during 10–11 hpf, suggesting RA acts upstream of scl to control primitive Myelopoiesis. However, the RA treatment blocks the increased primitive Myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive Myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Consistently, overexpressing gata4/6 inhibits aldh1a2 expression whereas depleting gata4/5/6 increases aldh1a2 expression. The results reveal that RA signaling acts downstream of gata4/5/6 to control primitive Myelopoiesis. But, 4-diethylamino-benzaldehyde fails to rescue the defective primitive Myelopoiesis in either cloche embryos or lycat morphants. Taken together, our results demonstrate that RA signaling restricts zebrafish primitive Myelopoiesis through acting downstream of gata4/5/6, upstream of, or parallel to, cloche, and upstream of scl.
Jihua Yao - One of the best experts on this subject based on the ideXlab platform.
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zebrafish microrna mir 210 5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mrnas downstream of gata4 5 6 transcription factor genes
Journal of Biological Chemistry, 2019Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua Yao, Qingshun ZhaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
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Zebrafish microRNA miR-210-5p inhibits primitive Myelopoiesis by silencing foxj1b and slc3a2a mRNAs downstream of gata4/5/6 transcription factor genes
Journal of Biological Chemistry, 2018Co-Authors: Wenshuang Jia, Dong Liang, Meijing Liu, Zhangji Dong, Xiaohua Dong, Yunyun Yue, Jihua YaoAbstract:Zebrafish gata4/5/6 genes encode transcription factors that lie on the apex of the regulatory hierarchy in primitive Myelopoiesis. However, little is known about the roles of microRNAs in gata4/5/6-regulated processes. Performing RNA-Seq deep sequencing analysis of the expression changes of microRNAs in gata4/5/6-knockdown embryos, we identified miR-210-5p as a regulator of zebrafish primitive Myelopoiesis. Knocking down gata4/5/6 (generating gata5/6 morphants) significantly increased miR-210-5p expression, whereas gata4/5/6 overexpression greatly reduced its expression. Consistent with inhibited primitive Myelopoiesis in the gata5/6 morphants, miR-210-5p overexpression repressed primitive Myelopoiesis, indicated by reduced numbers of granulocytes and macrophages. Moreover, knocking out miR-210 partially rescued the defective primitive Myelopoiesis in zebrafish gata4/5/6-knockdown embryos. Furthermore, we show that the restrictive role of miR-210-5p in zebrafish primitive Myelopoiesis is due to impaired differentiation of hemangioblast into myeloid progenitor cells. By comparing the set of genes with reduced expression levels in the gata5/6 morphants to the predicted target genes of miR-210-5p, we found that foxj1b and slc3a2a, encoding a forkhead box transcription factor and a solute carrier family 3 protein, respectively, are two direct downstream targets of miR-210-5p that mediate its inhibitory roles in zebrafish primitive Myelopoiesis. In summary, our results reveal that miR-210-5p has an important role in the genetic network controlling zebrafish primitive Myelopoiesis.
