Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal
Chromodomain helicase/ATPase DNA binding protein 1-like gene (Chd1l) participates in chromatin-dependent processes, including transcriptional activation and DNA repair. In this study, we have found for the first time that Chd1l is mainly expressed in the testicular tissues of prepubertal and adult m...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Stem Cells International |
| Online Access: | http://dx.doi.org/10.1155/2016/4069543 |
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| author | Shan-Shan Liu Yin-Shan Bai Li Feng Wen-Wei Dong Yang Li Li-Ping Xu Ning-Fang Ma |
| author_facet | Shan-Shan Liu Yin-Shan Bai Li Feng Wen-Wei Dong Yang Li Li-Ping Xu Ning-Fang Ma |
| author_sort | Shan-Shan Liu |
| collection | DOAJ |
| description | Chromodomain helicase/ATPase DNA binding protein 1-like gene (Chd1l) participates in chromatin-dependent processes, including transcriptional activation and DNA repair. In this study, we have found for the first time that Chd1l is mainly expressed in the testicular tissues of prepubertal and adult mice and colocalized with PLZF, OCT4, and GFRα1 in the neonatal mouse testis and THY1+ undifferentiated spermatogonia or spermatogonial stem cells (SSCs). Knockdown of endogenous Chd1l in cultured mouse undifferentiated SSCs inhibited the expression levels of Oct4, Plzf, Gfrα1, and Pcna genes, suppressed SSC colony formation, and reduced BrdU incorporation, while increasing SSC apoptosis. Moreover, the Chd1l gene expression is activated by GDNF in the cultured mouse SSCs, and the GDNF signaling pathway was modulated by endogenous levels of Chd1l; as demonstrated by the gene expression levels of GDNF, inducible transcripts Etv5, Bcl6b, Pou3f, and Lhx1, but not that of GDNF-independent gene, Taf4b, were significantly downregulated by Chd1l knockdown in mouse SSCs. Taken together, this study provides the first evidence to support the notion that Chd1l is an intrinsic and novel regulator for SSC survival and self-renewal, and it exerts such regulation at least partially through a GDNF signaling pathway. |
| format | Article |
| id | doaj-art-4423f5cf33ae40ad8e1814ad09b02fec |
| institution | Kabale University |
| issn | 1687-966X 1687-9678 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Stem Cells International |
| spelling | doaj-art-4423f5cf33ae40ad8e1814ad09b02fec2025-02-03T07:26:01ZengWileyStem Cells International1687-966X1687-96782016-01-01201610.1155/2016/40695434069543Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-RenewalShan-Shan Liu0Yin-Shan Bai1Li Feng2Wen-Wei Dong3Yang Li4Li-Ping Xu5Ning-Fang Ma6Department of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaDepartment of Histology and Embryology, Guangzhou Medical University, Guangzhou, ChinaChromodomain helicase/ATPase DNA binding protein 1-like gene (Chd1l) participates in chromatin-dependent processes, including transcriptional activation and DNA repair. In this study, we have found for the first time that Chd1l is mainly expressed in the testicular tissues of prepubertal and adult mice and colocalized with PLZF, OCT4, and GFRα1 in the neonatal mouse testis and THY1+ undifferentiated spermatogonia or spermatogonial stem cells (SSCs). Knockdown of endogenous Chd1l in cultured mouse undifferentiated SSCs inhibited the expression levels of Oct4, Plzf, Gfrα1, and Pcna genes, suppressed SSC colony formation, and reduced BrdU incorporation, while increasing SSC apoptosis. Moreover, the Chd1l gene expression is activated by GDNF in the cultured mouse SSCs, and the GDNF signaling pathway was modulated by endogenous levels of Chd1l; as demonstrated by the gene expression levels of GDNF, inducible transcripts Etv5, Bcl6b, Pou3f, and Lhx1, but not that of GDNF-independent gene, Taf4b, were significantly downregulated by Chd1l knockdown in mouse SSCs. Taken together, this study provides the first evidence to support the notion that Chd1l is an intrinsic and novel regulator for SSC survival and self-renewal, and it exerts such regulation at least partially through a GDNF signaling pathway.http://dx.doi.org/10.1155/2016/4069543 |
| spellingShingle | Shan-Shan Liu Yin-Shan Bai Li Feng Wen-Wei Dong Yang Li Li-Ping Xu Ning-Fang Ma Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal Stem Cells International |
| title | Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal |
| title_full | Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal |
| title_fullStr | Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal |
| title_full_unstemmed | Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal |
| title_short | Identification of CHD1L as an Important Regulator for Spermatogonial Stem Cell Survival and Self-Renewal |
| title_sort | identification of chd1l as an important regulator for spermatogonial stem cell survival and self renewal |
| url | http://dx.doi.org/10.1155/2016/4069543 |
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