Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4
Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation...
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MDPI AG
2018-03-01
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author | Alicja Dolzblasz Edyta M. Gola Katarzyna Sokołowska Elwira Smakowska-Luzan Adriana Twardawska Hanna Janska |
author_facet | Alicja Dolzblasz Edyta M. Gola Katarzyna Sokołowska Elwira Smakowska-Luzan Adriana Twardawska Hanna Janska |
author_sort | Alicja Dolzblasz |
collection | DOAJ |
description | Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the impacts of the internal oxidative stress on SAM and RAM functioning, we study the expression of selected meristem-specific (STM, CLV3, WOX5) and cell cycle-related (e.g., CYCB1, CYCD3;1) genes at the level of the promoter activity and/or transcript abundance in wild-type and loss-of-function ftsh4-1 mutant plants grown at 30 °C. In addition, we monitor cell cycle progression directly in apical meristems and analyze the responsiveness of SAM and RAM to plant hormones. We show that growth arrest in the ftsh4-1 mutant is caused by cell cycle dysregulation in addition to the loss of stem cell identity. Both the SAM and RAM gradually lose their proliferative activity, but with different timing relative to CYCB1 transcriptional activity (a marker of G2-M transition), which cannot be compensated by exogenous hormones. |
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format | Article |
id | doaj.art-24420a79b37d45279b74f64decc2c392 |
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issn | 1422-0067 |
language | English |
last_indexed | 2024-04-13T18:10:57Z |
publishDate | 2018-03-01 |
publisher | MDPI AG |
record_format | Article |
series | International Journal of Molecular Sciences |
spelling | doaj.art-24420a79b37d45279b74f64decc2c3922022-12-22T02:35:52ZengMDPI AGInternational Journal of Molecular Sciences1422-00672018-03-0119385310.3390/ijms19030853ijms19030853Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4Alicja Dolzblasz0Edyta M. Gola1Katarzyna Sokołowska2Elwira Smakowska-Luzan3Adriana Twardawska4Hanna Janska5Faculty of Biological Sciences, Institute of Experimental Biology, Kanonia 6/8, 50-328 Wroclaw, PolandFaculty of Biological Sciences, Institute of Experimental Biology, Kanonia 6/8, 50-328 Wroclaw, PolandFaculty of Biological Sciences, Institute of Experimental Biology, Kanonia 6/8, 50-328 Wroclaw, PolandFaculty of Biotechnology, University of Wroclaw, F. Joliot-Curie 14A, 50-383 Wroclaw, PolandFaculty of Biological Sciences, Institute of Experimental Biology, Kanonia 6/8, 50-328 Wroclaw, PolandFaculty of Biotechnology, University of Wroclaw, F. Joliot-Curie 14A, 50-383 Wroclaw, PolandShoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the impacts of the internal oxidative stress on SAM and RAM functioning, we study the expression of selected meristem-specific (STM, CLV3, WOX5) and cell cycle-related (e.g., CYCB1, CYCD3;1) genes at the level of the promoter activity and/or transcript abundance in wild-type and loss-of-function ftsh4-1 mutant plants grown at 30 °C. In addition, we monitor cell cycle progression directly in apical meristems and analyze the responsiveness of SAM and RAM to plant hormones. We show that growth arrest in the ftsh4-1 mutant is caused by cell cycle dysregulation in addition to the loss of stem cell identity. Both the SAM and RAM gradually lose their proliferative activity, but with different timing relative to CYCB1 transcriptional activity (a marker of G2-M transition), which cannot be compensated by exogenous hormones.http://www.mdpi.com/1422-0067/19/3/853Arabidopsiscell divisionsmitochondriaoxidative stressroot apical meristemshoot apical meristem |
spellingShingle | Alicja Dolzblasz Edyta M. Gola Katarzyna Sokołowska Elwira Smakowska-Luzan Adriana Twardawska Hanna Janska Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 International Journal of Molecular Sciences Arabidopsis cell divisions mitochondria oxidative stress root apical meristem shoot apical meristem |
title | Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 |
title_full | Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 |
title_fullStr | Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 |
title_full_unstemmed | Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 |
title_short | Impairment of Meristem Proliferation in Plants Lacking the Mitochondrial Protease AtFTSH4 |
title_sort | impairment of meristem proliferation in plants lacking the mitochondrial protease atftsh4 |
topic | Arabidopsis cell divisions mitochondria oxidative stress root apical meristem shoot apical meristem |
url | http://www.mdpi.com/1422-0067/19/3/853 |
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