In penaeids, the major yolk protein precursor vitellogenin is synthesized in both the hepatopancreas and the ovary. While ovarian vitellogenin expression is clearly regulated by hormones from the X-organ/sinus gland in the eyestalk, regulation in the hepatopancreas remains poorly understood. Here, we performed
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In penaeids, the major yolk protein precursor vitellogenin is synthesized in both the hepatopancreas and the ovary. While ovarian vitellogenin expression is clearly regulated by hormones from the X-organ/sinus gland in the eyestalk, regulation in the hepatopancreas remains poorly understood. Here, we performed transcriptome profiling stratified by endogenous hepatopancreatic vitellogenin gene (
Maj-Vg1) expression levels in immature kuruma prawn
Marsupenaeus japonicus. Pathway enrichment analysis identified the insulin, mechanistic target of rapamycin (mTOR), glucagon, and AMP-activated protein kinase (AMPK) pathways as candidate modules associated with the control of hepatopancreatic
Maj-Vg1 expression. Analysis of differentially expressed genes identified
slit-like (
Slit) and
calreticulin (
Calr) as genes potentially involved in the regulation of
Maj-Vg1 expression. In ex vivo hepatopancreas explants, insulin-like peptide 1 from this species induced
Maj-Vg1 and was accompanied by the upregulation of lipogenic markers (
Max-like protein X (
Mlx) and
acetyl-CoA carboxylase (
Acc)), consistent with vitellogenin’s lipid-transport role. Expression patterns of
Calr,
tuberous sclerosis complex 1 and
2 (
Tsc1 and
Tsc2) suggest regulatory inputs beyond insulin signaling, indicating context-dependent regulation. Taken together, these data identify metabolic status as an important contributor to hepatopancreatic
Maj-Vg1 expression and define further research targets, including mTOR, AMPK, glucagon, and the Slit/Roundabout axis, for understanding vitellogenesis in penaeids.
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