Programmed cell death in the tobacco hornworm, Manduca sexta: alteration in protein synthesis

Z Zakeri1, D Quaglino, T Latham

  • 1Department of Biology, Queens College, Flushing, New York 11367, USA.

Insights

The labial glands of the tobacco hornworm (Manduca sexta) undergo programmed cell death during metamorphosis. Early events include reduced protein synthesis and lysosomal activation, but the precise mechanism for synthesis shutdown is still unknown.

Area of Science:

  • Developmental biology
  • Cell biology
  • Insect physiology

Background:

  • The labial glands of Manduca sexta undergo programmed cell death during the larva-to-pupa transition.
  • Understanding the molecular mechanisms of this metamorphic cell death is crucial for insect development studies.

Purpose of the Study:

  • To investigate the early cellular events and molecular changes associated with labial gland cell death during Manduca sexta metamorphosis.
  • To elucidate the mechanisms regulating protein synthesis suppression during this developmental process.

Main Methods:

  • Analysis of protein synthesis rates.
  • Monitoring of specific mRNA levels.
  • Examination of cellular structures, including the endoplasmic reticulum.
  • Assay of lysosomal enzyme activity (acid phosphatase).

Main Results:

  • Metamorphic death of labial glands occurs over a 4-day period.
  • Earliest changes include a sharp decrease in protein synthesis and selective mRNA regulation.
  • Early rearrangement of the rough endoplasmic reticulum was observed.
  • Lysosomal acid phosphatase activity increased, leading to autophagic destruction of cytoplasm.
  • Lysosome activation did not fully explain the reduced protein synthesis.

Conclusions:

  • Programmed cell death in Manduca sexta labial glands involves early suppression of protein synthesis and lysosomal activation.
  • The precise mechanism causing the generalized decrease in protein synthesis remains to be fully elucidated.
  • Further research is needed to identify the signaling pathways responsible for inhibiting protein synthesis during metamorphosis.