DOI: 10.5061/dryad.8w9ghx417
title: TGFβRI modulates metabolic reprogramming via the aPKC-PEPCK axis during pupal diapause in the cotton Bollworm, <em>Helicoverpa armigera</em>

description: Insect diapause represents an evolutionarily conserved developmental
 arrest strategy characterized by profound metabolic suppression, though
 its underlying regulatory mechanisms remain incompletely elucidated. In
 this study, we identify a crucial signaling cascade involving transforming
 growth factor β receptor I (TGFβRI), atypical protein kinase C (aPKC), and
 phosphoenolpyruvate carboxykinase (PEPCK) that orchestrates metabolic
 reprogramming during pupal diapause in Helicoverpa armigera.
 Temporospatial expression profiling revealed coordinated downregulation of
 TGFβRI and PEPCK, a key gluconeogenic enzyme in diapause-destined pupae.
 Overexpression of TGFβRI was found to increase PEPCK levels in Helicoverpa
 zea ovarian cells (HzAm1). Concordantly, treatment of nondiapause-destined
 pupae with SB431542, a TGFβRI inhibitor, suppressed PEPCK in a
 dose-dependent manner. Further analysis revealed that aPKC serves as a
 downstream effector, as its phosphorylation levels were notably elevated
 in nondiapause-destined pupae, corresponding to TGFβRI activity. Notably,
 TGFβRI selectively regulates aPKC phosphorylation without altering total
 protein levels. Disrupting aPKC, either through RNAi-mediated knockdown or
 pharmacological inhibition (Go6983), robustly diminished PEPCK expression
 both in vitro and in vivo, and crucially delayed pupal development.
 Evolutionary analysis uncovered 50–70% sequence conservation of aPKC
 across Lepidoptera, highlighting its regulatory significance. Taken
 together, our findings elucidate a TGFβRI/aPKC/PEPCK axis that couples
 developmental signaling with metabolic regulation during insect diapause,
 offering mechanistic insights into this adaptive survival strategy.
description: # TGFβRI Modulates Metabolic Reprogramming via the aPKC-PEPCK Axis During
 Pupal Diapause in the Cotton Bollworm, Helicoverpa armigera Dataset DOI:
 [10.5061/dryad.8w9ghx417](https://doi.org/10.5061/dryad.8w9ghx417) ##
 Description of the data and file structure ### Files and variables ####
 File: Fig1__2__3__6__7_WB_Raw_data.pdf **Description:** We have integrated
 the original images and added corresponding descriptions, and provided a
 PDF file to prevent display position deviation. Fig. 1.(A) Overexpression
 of H. armigera TGFβRI upregulates PEPCK in HzAm1 cells. Fig. 1.(B)
 Injection of TGFβRI inhibitor SB431542 (SB) downregulates H.
 armigera PEPCK in nondiapause pupae. Fig. 2. (A) aPKC protein expression
 dynamics in diapause destined (DP) and nondiapause-destined (NP) pupae.
 Fig. 2. (B) p-aPKC (Thr410/403) protein expression dynamics in
 diapause destined (DP) and nondiapause-destined (NP) pupae. Fig. 3. (A)
 aPKC protein levels in diapause pupae following 20-hydroxyecdysone (20E)
 injection. Fig. 3. (B) p-aPKC (Thr410/403) protein levels in diapause
 pupae following 20-hydroxyecdysone (20E) injection.  Fig. 6. (A)
 aPKC levels following TGFβRI overexpression. Fig. 6. (B) p-aPKC levels
 following TGFβRI overexpression. Fig. 6. (C) p-aPKC levels after injection
 of TGFβRI inhibitor SB431542 (SB) in day 6-7 nondiapause pupae. Fig. 7.
 (A) aPKC levels following aPKC knockdown. Fig. 7. (B) PEPCK levels
 following aPKC knockdown. Fig. 7. (C) Dose-dependent PEPCK inhibition by
 aPKC inhibitor Go6983 in cells. Fig. 7. (D) Dose-dependent PEPCK
 inhibition by aPKC inhibitor Go6983 in pupae.  #### File:
 Fig._8_Eyespot_migration.csv **Description:** Fig. 8. Developmental delay
 induced by aPKC inhibition in *H. armigera* pupae. ## Code/software You
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