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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Plant Sci. | doi: 10.3389/fpls.2019.01198

The function of autophagy in lace plant programmed cell death

  • 1Swedish University of Agricultural Sciences, Sweden
  • 2Dalhousie University, Canada
  • 3University of Prince Edward Island, Canada

The lace plant (Aponogeton madagascariensis) is an aquatic monocot that utilizes programmed cell death (PCD) to form perforations throughout its mature leaves as part of normal development. The lace plant is an emerging model system representing a unique form of developmental PCD. The role of autophagy in lace plant PCD was investigated using live cell imaging, transmission electron microscopy (TEM), immunolocalization, and in vivo pharmacological experimentation. ATG8 immunostaining and acridine orange staining revealed that autophagy occurs in both healthy and dying cells. Autophagosome-like vesicles were also found in healthy and dying cells through ultrastructural analysis with TEM. Following autophagy modulation, there was a noticeable increase in vesicles and vacuolar aggregates. A novel cell death assay utilizing lace plant leaves revealed that autophagy enhancement with rapamycin significantly decreased cell death rates compared to the control, whereas inhibition of autophagosome formation with wortmannin or blocking the degradation of cargoes with concanamycin A had an opposite effect. Although autophagy modulation significantly affected cell death rates in cells that are destined to die, neither the promotion nor inhibition of autophagy in whole plants had a significant effect on the number of perforations formed in lace plant leaves. Our data indicate that autophagy predominantly contributes to cell survival and we found no clear evidence for its direct involvement in the induction of developmental PCD during perforation formation in lace plant leaves.

Keywords: programmed cell death, Autophagy, leaf development, Perforation formation, live cell imaging

Received: 13 May 2019; Accepted: 30 Aug 2019.

Copyright: © 2019 Dauphinee, Denbigh, Rollini, Fraser, Lacroix and Gunawardena. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Arunika H. Gunawardena, Dalhousie University, Halifax, B3H 4R2, Nova Scotia, Canada, arunika.gunawardena@dal.ca