Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development.
Numerous studies using cultured mammalian cells have shown that the three GGAs (Golgi-localized, gamma-ear containing, ADP-ribosylation factor- binding proteins) function in the transport of cargo proteins between the trans- Golgi network and endosomes. However, the in vivo role(s) of these adaptor...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3266899?pdf=render |
| _version_ | 1818019258515324928 |
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| author | Jennifer Govero Balraj Doray Hongdong Bai Stuart Kornfeld |
| author_facet | Jennifer Govero Balraj Doray Hongdong Bai Stuart Kornfeld |
| author_sort | Jennifer Govero |
| collection | DOAJ |
| description | Numerous studies using cultured mammalian cells have shown that the three GGAs (Golgi-localized, gamma-ear containing, ADP-ribosylation factor- binding proteins) function in the transport of cargo proteins between the trans- Golgi network and endosomes. However, the in vivo role(s) of these adaptor proteins and their possible functional redundancy has not been analyzed. In this study, the genes encoding GGAs1-3 were disrupted in mice by insertional mutagenesis. Loss of GGA1 or GGA3 alone was well tolerated whereas the absence of GGA2 resulted in embryonic or neonatal lethality, depending on the genetic background of the mice. Thus, GGA2 mediates a vital function that cannot be compensated for by GGA1and/or GGA3. The combined loss of GGA1 and GGA3 also resulted in a high incidence of neonatal mortality but in this case the expression level of GGA2 may be inadequate to compensate for the loss of the other two GGAs. We conclude that the three mammalian GGAs are essential proteins that are not fully redundant. |
| first_indexed | 2024-04-14T07:50:25Z |
| format | Article |
| id | doaj.art-8b7cec6590c84d559fa51f27c2b71476 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-14T07:50:25Z |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-8b7cec6590c84d559fa51f27c2b714762022-12-22T02:05:13ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0171e3018410.1371/journal.pone.0030184Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development.Jennifer GoveroBalraj DorayHongdong BaiStuart KornfeldNumerous studies using cultured mammalian cells have shown that the three GGAs (Golgi-localized, gamma-ear containing, ADP-ribosylation factor- binding proteins) function in the transport of cargo proteins between the trans- Golgi network and endosomes. However, the in vivo role(s) of these adaptor proteins and their possible functional redundancy has not been analyzed. In this study, the genes encoding GGAs1-3 were disrupted in mice by insertional mutagenesis. Loss of GGA1 or GGA3 alone was well tolerated whereas the absence of GGA2 resulted in embryonic or neonatal lethality, depending on the genetic background of the mice. Thus, GGA2 mediates a vital function that cannot be compensated for by GGA1and/or GGA3. The combined loss of GGA1 and GGA3 also resulted in a high incidence of neonatal mortality but in this case the expression level of GGA2 may be inadequate to compensate for the loss of the other two GGAs. We conclude that the three mammalian GGAs are essential proteins that are not fully redundant.http://europepmc.org/articles/PMC3266899?pdf=render |
| spellingShingle | Jennifer Govero Balraj Doray Hongdong Bai Stuart Kornfeld Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. PLoS ONE |
| title | Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. |
| title_full | Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. |
| title_fullStr | Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. |
| title_full_unstemmed | Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. |
| title_short | Analysis of Gga null mice demonstrates a non-redundant role for mammalian GGA2 during development. |
| title_sort | analysis of gga null mice demonstrates a non redundant role for mammalian gga2 during development |
| url | http://europepmc.org/articles/PMC3266899?pdf=render |
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