Next Article in Journal
Green Ferrate(VI) for Multiple Treatments of Fracturing Wastewater: Demulsification, Visbreaking, and Chemical Oxygen Demand Removal
Previous Article in Journal
Therapeutic Effect of Dipsacus asperoides C. Y. Cheng et T. M. Ai in Ovalbumin-Induced Murine Model of Asthma
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2019, 20(8), 1856; https://doi.org/10.3390/ijms20081856

Identification and Characterization of Four Autophagy-Related Genes That Are Expressed in Response to Hypoxia in the Brain of the Oriental River Prawn (Macrobrachium nipponense)

1
Wuxi Fishery College, Nanjing Agricultural University, Wuxi 214081, China
2
Key Laboratory of Freshwater Fisheries and Germplasm Resources Use, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China
3
Tianjin Fisheries Research Institute, Tianjin 300221, China
4
Key Laboratory of Exploration and Use of Aquatic Genetic Resources, Shanghai Ocean University, Shanghai 201306, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to the work.
Received: 20 March 2019 / Revised: 1 April 2019 / Accepted: 11 April 2019 / Published: 15 April 2019
(This article belongs to the Special Issue Adaptation to Hypoxia: A Chimera?)
  |  
PDF [11753 KB, uploaded 15 April 2019]
  |  

Abstract

Autophagy is a cytoprotective mechanism triggered in response to adverse environmental conditions. Herein, we investigated the autophagy process in the oriental river prawn (Macrobrachium nipponense) following hypoxia. Full-length cDNAs encoding autophagy-related genes (ATGs) ATG3, ATG4B, ATG5, and ATG9A were cloned, and transcription following hypoxia was explored in different tissues and developmental stages. The ATG3, ATG4B, ATG5, and ATG9A cDNAs include open reading frames encoding proteins of 319, 264, 268, and 828 amino acids, respectively. The four M. nipponense proteins clustered separately from vertebrate homologs in phylogenetic analysis. All four mRNAs were expressed in various tissues, with highest levels in brain and hepatopancreas. Hypoxia up-regulated all four mRNAs in a time-dependent manner. Thus, these genes may contribute to autophagy-based responses against hypoxia in M. nipponense. Biochemical analysis revealed that hypoxia stimulated anaerobic metabolism in the brain tissue. Furthermore, in situ hybridization experiments revealed that ATG4B was mainly expressed in the secretory and astrocyte cells of the brain. Silencing of ATG4B down-regulated ATG8 and decreased cell viability in juvenile prawn brains following hypoxia. Thus, autophagy is an adaptive response protecting against hypoxia in M. nipponense and possibly other crustaceans. Recombinant MnATG4B could interact with recombinant MnATG8, but the GST protein could not bind to MnATG8. These findings provide us with a better understanding of the fundamental mechanisms of autophagy in prawns. View Full-Text
Keywords: Autophagy; Hypoxia; Macrobrachium nipponense; Brain; RNA interference Autophagy; Hypoxia; Macrobrachium nipponense; Brain; RNA interference
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Sun, S.; Wu, Y.; Fu, H.; Ge, X.; You, H.; Wu, X. Identification and Characterization of Four Autophagy-Related Genes That Are Expressed in Response to Hypoxia in the Brain of the Oriental River Prawn (Macrobrachium nipponense). Int. J. Mol. Sci. 2019, 20, 1856.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top