摘要： Mitochondria play an important role in maintaining metabolic and energy homeostasis in the plant cell. Thus, perturbation of mitochondrial structure and function will affect plant growth and development. Arabidopsis slow growth3 (slo3) is defective in At3g61360 that encodes a pentatricopeptide repeat (PPR) protein. Analysis of slo3 mitochondrial RNA metabolism revealed that the splicing of nad7 intron 2 is impaired, which leads to a dramatic reduction in complex I activity. So the SLO3 PPR protein is a splicing factor that is required for the removal of nad7 intron 2 in Arabidopsis. The slo3 mutant plants have obvious phenotypes with severe growth retardation and delayed development. The size of root apical meristem (RAM) is reduced and the production of meristem cells is decreased in slo3. Furthermore, the rosette leaves of slo3 are curled or crinkled, which may be derived from uneven growth of the leaf surface. The underlying mechanisms by which dysfunctional mitochondria affect these growth and developmental phenotypes have yet to be established. Nonetheless, plant hormone auxin is known to play an important role in orchestrating the development of RAM and leaf shape. It is possible that dysfunctional mitochondria may interact with auxin signaling pathways to regulate the boundary of RAM and the cell division arrest front during leaf growth in Arabidopsis. 其他題名： Plant Signal Behav 出版者： United States: Taylor & Francis 出版日期： 2015-10-03 出處： Plant signaling & behavior, 2015-10, Vol.10 (10), p.e1071002 資源來源： Taylor & Francis Online 版權： 2015 Taylor & Francis Group, LLC 2015 版權： 2015 Taylor & Francis Group, LLC 2015 Taylor & Francis Group, LLC 識別號： ISSN: 1559-2316 識別號： ISSN: 1559-2324 識別號： EISSN: 1559-2324 識別號： DOI: 10.1080/15592324.2015.1071002 識別號： PMID: 26237004
