When the surrounding water dilutes, a shrimp’s cells face a triple assault. Osmotic stress makes cells swell as water rushes in, disrupting the delicate water balance inside tissues. Ionic stress impairs the channels and enzymes that keep sodium, potassium and chloride in check. And oxidative stress generates reactive oxygen species that oxidize proteins, inactivate enzymes and damage DNA. Together, these pressures can trigger apoptosis, alter membrane fluidity and ultimately kill the animal. Understanding how shrimp blunt this cascade is not just an academic exercise; it directly determines survival, growth and productivity on farms that supply a large share of the world’s seafood protein.

The review’s first major theme is how shrimp perceive salinity change in the first place. G protein-coupled receptors, or GPCRs, are abundant in penaeid genomes: the L. vannamei reference genome contains 457 GPCR genes, and transcriptome curation in P. monodon identified three major classes totaling 350 members. Intriguingly, the authors caution that direct evidence for GPCRs acting as primary salinity sensors remains limited. Instead, these receptors are more plausibly engaged indirectly, as salinity shifts alter the availability of neuroendocrine and paracrine ligands. Once activated, GPCRs funnel signals through cAMP, protein kinase A, PI3K-Akt and MAPK cascades. Transcriptomic profiling of P. monodon gills under chronic low salinity showed differentially expressed genes mapping to PI3K-Akt, MAPK and calcium signaling pathways, supporting a role for GPCR-linked cascades in gill-centered osmoregulatory acclimation.

Calcium signaling emerges as a second, faster perception module. As extracellular osmotic pressure drops, calcium-permeable membrane channels open and calcium is also mobilized from intracellular stores such as the endoplasmic reticulum, producing a transient spike in cytosolic calcium. In P. monodon, acute low-salt stress significantly enriches gene sets for calcium ion transmembrane transport, calmodulin binding and regulation of cytosolic calcium concentration, accompanied by increased activity of Ca2+/Mg2+-ATPase. The calcium wave activates a battery of calcium-sensitive kinases and phosphatases that fine-tune ion pumps through phosphorylation, restoring not only calcium balance but also sodium and potassium equilibrium. Strikingly, the cellular energy sensor AMPK rides along: hepatopancreatic AMPK-alpha transcripts increase roughly 28-fold just six hours after Pacific white shrimp are transferred from salinity 20 to salinity 3, linking osmotic calcium dynamics to metabolic reprogramming through calcium/calmodulin-dependent kinase kinase pathways.

The third perception layer is phospholipid signaling and membrane remodeling. Low salinity directly changes the physical state of cell membranes, particularly their fluidity and the activity of embedded proteins. Shrimp respond by adjusting membrane phospholipid composition, and over longer exposures they shift the ratio of saturated to unsaturated fatty acids to keep membranes supple. Phospholipase C-mediated hydrolysis of phosphoinositides generates second messengers such as IP3 and diacylglycerol, tuning membrane-protein interactions and the trafficking of ion-transport systems. The review frames this lipid turnover primarily as membrane remodeling that stabilizes integrity and preserves the function of osmoregulatory channels and pumps during cell swelling and volume recovery, a subtle but crucial distinction for interpreting the data.

Downstream of perception, three kinase networks translate stress signals into coordinated action. The MAPK pathway, with its ERK, JNK and p38 branches, governs cell growth, stress-responsive transcription and apoptosis; ERK supports proliferation while JNK and p38 can eliminate severely damaged cells and regulate inflammatory gene expression. The PI3K-Akt pathway acts as a survival engine: activated PI3K generates PIP3, which engages Akt, which in turn phosphorylates mTOR to promote anabolic metabolism while suppressing apoptotic proteins such as Bad and excluding FOXO transcription factors from the nucleus. Negative feedback through PTEN keeps the pathway from pathological overactivation. Meanwhile, the NF-kappaB pathway, engaged via I-kappa-B regulation and nuclear translocation, promotes immune, stress-response and anti-apoptotic gene programs. Together these modules drive gill-centered osmoregulation, immune priming and antioxidant control.

At the organ level, the gills take center stage. Gill ionocytes dynamically adjust ion absorption or excretion through core transport systems, most notably Na+/K+-ATPase and carbonic anhydrase. In dilute water, P. monodon ramps up ion uptake to raise internal osmotic pressure and prevent excessive water influx and cellular rupture. Na+/K+-ATPase burns ATP to exchange three sodium ions for two potassium ions across the membrane, maintaining the electrochemical gradient, and its activity typically rises under low salinity. Carbonic anhydrase catalyzes the reversible hydration of carbon dioxide, producing bicarbonate and protons that support the Na+/H+ exchanger and acid-base balance. Recent transcriptome work in P. monodon found markedly upregulated Na+/K+-ATPase subunits and elevated carbonic anhydrase transcripts under low salinity, alongside dynamic changes in actin and tubulin genes indicating cytoskeletal remodeling of gill epithelia. Antennal and maxillary glands contribute auxiliary water and ion excretion, though shrimp-specific mechanistic data for the latter remain thin.

The review also highlights two cellular quality-control systems that have received less attention. Autophagy, the degradation and recycling of damaged proteins and organelles, is initiated when energy stress activates AMPK and relieves mTOR-mediated inhibition of the Atg1 initiation complex. A cascade of Atg proteins, including the transmembrane Atg9 and the Atg7-Atg3 conjugation machinery that lipidates Atg8, builds autophagosomes that fuse with lysosomes to recycle cellular debris. In parallel, endoplasmic reticulum stress engages three sensor arms: PERK slows protein synthesis by phosphorylating eIF2-alpha while activating ATF4; ATF6 is cleaved in the Golgi to activate ER quality-control genes; and IRE1 splices XBP1 mRNA to boost chaperone and lipid biosynthesis. Proteins such as GRP78/BiP and CHOP decide whether the cell restores folding capacity or succumbs to apoptosis.

Salinity stress also reshapes immunity and redox balance. Under hyposalinity, shrimp upregulate scleroproteins that thicken the cuticle, lysozymes that dissolve bacterial cell walls, and antilipopolysaccharide factors that neutralize bacterial endotoxin. Recent transcriptomic data from P. monodon show that low salinity alone triggers upregulation of Toll-like receptor genes and downstream NF-kappaB components, suggesting osmotic stress primes innate immunity even without pathogens. Because immune effector processes and osmotic disturbance both elevate reactive oxygen species, antioxidant defense is tightly coupled to immune function. The Keap1-Nrf2 axis sits at the center: oxidative stress releases Nrf2 from Keap1, allowing it to enter the nucleus and bind antioxidant response elements, switching on superoxide dismutase, catalase, glutathione peroxidase and heme oxygenase-1, with feedback mechanisms preventing an overactive response.

The practical payoff is already visible in feeding trials. The review compiles nutritional interventions with direct experimental support for improved low-salinity resilience: cholesterol and phospholipids to stabilize membranes, vitamin C derivatives such as L-ascorbyl-2-polyphosphate to buffer oxidation, potassium and magnesium supplementation to enhance ion balance, and myo-inositol to support stress tolerance. Looking forward, the authors argue that identifying the true upstream osmosensors, integrating multi-omics with time-series designs, and exploiting chromosome-level genomes of L. vannamei, P. monodon and Marsupenaeus japonicus for comparative genomics and marker-assisted breeding will be essential. Genome editing remains technically difficult in crustaceans, so selective breeding and genomic selection carry near-term weight. As salinity fluctuations grow more frequent and less predictable, decoding the shrimp’s molecular playbook may prove decisive for building climate-resilient aquaculture systems.

Subject of Research: Molecular and physiological adaptations of penaeid shrimp to low-salinity stress

Article Title: Molecular and physiological adaptations to low-salinity stress in penaeid shrimp: a focus on Litopenaeus vannamei and Penaeus monodon

Article References: Huang, S., Zhou, F., Jiang, S., Li, E., & Li, Y. (2026). Molecular and physiological adaptations to low-salinity stress in penaeid shrimp: a focus on Litopenaeus vannamei and Penaeus monodon. Stress Biology, 6(1), Article 34. https://doi.org/10.1007/s44154-026-00295-4

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00295-4

Keywords: penaeid shrimp, Litopenaeus vannamei, Penaeus monodon, low-salinity stress, osmoregulation, GPCR signaling, calcium signaling, Na+/K+-ATPase, autophagy, endoplasmic reticulum stress, Nrf2 antioxidant pathway, aquaculture