# Transciptomic and histological analysis of hepatopancreas, muscle and gill tissues of oriental river prawn (Macrobrachium nipponense) in response to chronic hypoxia

**Authors:** Shengming Sun, Fujun Xuan, Hongtuo Fu, Jian Zhu, Xianping Ge, Zhimin Gu

PMC · DOI: 10.1186/s12864-015-1701-3 · 2015-07-03

## TL;DR

This study explores how the oriental river prawn adapts to low oxygen conditions by analyzing gene expression and tissue changes in key organs.

## Contribution

The study identifies differentially expressed genes and histological changes in prawn tissues under chronic hypoxia, offering insights for genetic improvement.

## Key findings

- 8,892 genes were up-regulated and 5,760 down-regulated in response to chronic hypoxia.
- DEGs were enriched in stress-related pathways like oxidative phosphorylation and glycolysis.
- Histological differences were observed in hepatopancreas and gills under hypoxia.

## Abstract

Oriental river prawn, Macrobrachium nipponense, is a commercially important species found in brackish and fresh waters throughout China. Chronic hypoxia is a major physiological challenge for prawns in culture, and the hepatopancreas, muscle and gill tissues play important roles in adaptive processes. However, the effects of dissolved oxygen availability on gene expression and physiological functions of those tissues of prawns are unknown. Adaptation to hypoxia is a complex process, to help us understand stress-sensing mechanism and ultimately permit selection for hypoxia- tolerant prawns, we performed transcriptomic analysis of juvenile M. nipponense hepatopancreas, gill and muscle tissues by RNA-Seq.

Approximately 46,472,741; 52,773,612 and 58,195,908 raw sequence reads were generated from hepatopancreas, muscle and gill tissues, respectively. A total of 62,722 unigenes were generated, of the assembled unigenes, we identified 8,892 genes that were significantly up-regulated, while 5,760 genes were significantly down-regulated in response to chronic hypoxia. Genes from well known functional categories and signaling pathways associated with stress responses and adaptation to extreme environments were significantly enriched, including genes in the functional categories “response to stimulus”, “transferase activity” and “oxidoreductase activity”, and the signaling pathways “oxidative phosphorylation”, “glycolysis/gluconeogenesis” and “MAPK signaling”. The expression patterns of 18 DEGs involved in hypoxic regulation of M. nipponense were validated by quantitative real-time reverse-transcriptase polymerase chain reactions (qRT-PCR; average correlation coefficient = 0.94). In addition, the hepatopancreas and gills exhibited histological differences between hypoxia and normoxia groups. These structural alterations could affect the vital physiological functions of prawns in response to chronic hypoxia, which could adversely affect growth and survival of M. nipponense.

Gene expression changes in tissues from the oriental river prawn provide a preliminary basis to better understand the molecular responses of M. nipponense to chronic hypoxia. The differentially expressed genes (DEGs) identified in M. nipponense under hypoxia stress may be important for future genetic improvement of cultivated prawns or other crustaceans through transgenic approaches aimed at increasing hypoxia tolerance.

The online version of this article (doi:10.1186/s12864-015-1701-3) contains supplementary material, which is available to authorized users.

## Linked entities

- **Species:** Macrobrachium nipponense (taxon 159736)

## Full-text entities

- **Genes:** NADH dehydrogenase subunit 1 [NCBI Gene 10200254], CCO I [NCBI Gene 10200256]
- **Diseases:** Hypoxic (MESH:D002534), NCR (MESH:D009336), hypertrophy (MESH:D006984), death (MESH:D003643), gill injury (MESH:C000654764), MEL (MESH:D008557), anoxia (MESH:D000860)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Macrobrachium nipponense (oriental river prawn, species) [taxon 159736]
- **Mutations:** 1A-C

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC4490754/full.md

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Source: https://tomesphere.com/paper/PMC4490754