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Structural variation between neuropeptide isoforms affects function in the lobster cardiac system.

Audrey J Muscato1, Daniel J Powell1, Warsameh Bulhan1

  • 1Biology Dept., Bowdoin College, 6500 College Station, Brunswick, ME 04011, USA.

General and Comparative Endocrinology
|May 27, 2022
PubMed
Summary
This summary is machine-generated.

Peptide isoforms, like lobster C-type allatostatins (AST-Cs), can elicit different physiological responses. Single amino acid changes, not C-terminal amidation, significantly alter these specific peptide signaling effects.

Keywords:
AllatostatinCrustaceaHeartbeatIsoformsNeuropeptideStructure–function

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Area of Science:

  • Neuroendocrinology
  • Comparative Physiology
  • Molecular Signaling

Background:

  • Neuronal responses depend on peptide-receptor binding.
  • Peptide isoforms can trigger distinct physiological outcomes through varied receptor interactions.
  • In American lobsters, C-type allatostatins (AST-Cs) modulate cardiac function, with AST-C II showing a unique response.

Purpose of the Study:

  • To identify sequence features responsible for differential AST-C isoform activity in the lobster cardiac system.
  • To investigate the role of C-terminal amidation and single amino acid substitutions in modulating peptide function.

Main Methods:

  • Chemical modification of native AST-C peptide sequences.
  • Analysis of altered peptide isoforms' effects on lobster cardiac parameters (frequency, force).

Main Results:

  • C-terminal amidation was not critical for AST-C activity in the lobster heart.
  • Single amino acid substitutions within the AST-C consensus sequence were found to significantly alter specific cardiac responses.
  • Differential binding affinities or receptor interactions are likely mediated by subtle sequence variations.

Conclusions:

  • Specific amino acid residues within the AST-C sequence are key determinants of differential cardiac responses.
  • Peptide sequence, rather than C-terminal amidation alone, dictates the nuanced physiological effects of AST-C isoforms.