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The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning
Leaves develop as planar organs, with a morphology that is specialized for photosynthesis. Development of a planar leaf requires genetic networks that set up opposing adaxial and abaxial sides of the leaf, which leads to establishment of dorsoventral polarity. While many genes have been identified t...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Oxford University Press
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430996/ https://www.ncbi.nlm.nih.gov/pubmed/22791832 http://dx.doi.org/10.1093/jxb/ers184 |
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author | Moschopoulos, Alexis Derbyshire, Paul Byrne, Mary E. |
author_facet | Moschopoulos, Alexis Derbyshire, Paul Byrne, Mary E. |
author_sort | Moschopoulos, Alexis |
collection | PubMed |
description | Leaves develop as planar organs, with a morphology that is specialized for photosynthesis. Development of a planar leaf requires genetic networks that set up opposing adaxial and abaxial sides of the leaf, which leads to establishment of dorsoventral polarity. While many genes have been identified that regulate adaxial and abaxial fate there is little information on how this is integrated with cellular function. EMBRYO DEFECTIVE DEVELOPMENT1 (EDD1) is a nuclear gene that encodes a plastid and mitochondrial localized glycyl-tRNA synthetase. Plants with partial loss of EDD1 function have changes in patterning of margin and distal regions of the leaf. In combination with mutations in the MYB domain transcription factor gene ASYMMETRIC LEAVES1 (AS1), partial loss of EDD1 function results in leaves with reduced adaxial fate. EDD1 may influence leaf dorsoventral polarity through regulating the abaxial fate genes KANADI1 (KAN1) and ETTIN (ETT)/AUXIN RESPONSE FACTOR3 (ARF3) since these genes are upregulated in the edd1 as1 double mutant. SCABRA3 (SCA3), a nuclear gene that encodes the plastid RNA polymerase is also required for leaf adaxial fate in the absence of AS1. These results add a novel component to networks of genetic regulation of leaf development and suggest that organelles, particularly plastids, are required in leaf patterning. Potentially, signalling from organelles is essential for coordination of different cell fates within the developing leaf. |
format | Online Article Text |
id | pubmed-3430996 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-34309962012-08-30 The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning Moschopoulos, Alexis Derbyshire, Paul Byrne, Mary E. J Exp Bot Research Paper Leaves develop as planar organs, with a morphology that is specialized for photosynthesis. Development of a planar leaf requires genetic networks that set up opposing adaxial and abaxial sides of the leaf, which leads to establishment of dorsoventral polarity. While many genes have been identified that regulate adaxial and abaxial fate there is little information on how this is integrated with cellular function. EMBRYO DEFECTIVE DEVELOPMENT1 (EDD1) is a nuclear gene that encodes a plastid and mitochondrial localized glycyl-tRNA synthetase. Plants with partial loss of EDD1 function have changes in patterning of margin and distal regions of the leaf. In combination with mutations in the MYB domain transcription factor gene ASYMMETRIC LEAVES1 (AS1), partial loss of EDD1 function results in leaves with reduced adaxial fate. EDD1 may influence leaf dorsoventral polarity through regulating the abaxial fate genes KANADI1 (KAN1) and ETTIN (ETT)/AUXIN RESPONSE FACTOR3 (ARF3) since these genes are upregulated in the edd1 as1 double mutant. SCABRA3 (SCA3), a nuclear gene that encodes the plastid RNA polymerase is also required for leaf adaxial fate in the absence of AS1. These results add a novel component to networks of genetic regulation of leaf development and suggest that organelles, particularly plastids, are required in leaf patterning. Potentially, signalling from organelles is essential for coordination of different cell fates within the developing leaf. Oxford University Press 2012-09 2012-07-12 /pmc/articles/PMC3430996/ /pubmed/22791832 http://dx.doi.org/10.1093/jxb/ers184 Text en © The Author [2012]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/bync/3.0/uk/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Moschopoulos, Alexis Derbyshire, Paul Byrne, Mary E. The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title | The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title_full | The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title_fullStr | The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title_full_unstemmed | The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title_short | The Arabidopsis organelle-localized glycyl-tRNA synthetase encoded by EMBRYO DEFECTIVE DEVELOPMENT1 is required for organ patterning |
title_sort | arabidopsis organelle-localized glycyl-trna synthetase encoded by embryo defective development1 is required for organ patterning |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430996/ https://www.ncbi.nlm.nih.gov/pubmed/22791832 http://dx.doi.org/10.1093/jxb/ers184 |
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