HOW DOES HEAT SHOCK AT 34 DEGREES CELSIUS AFFECT TBI IN C. ELEGANS WHEN COMPARED TO TBI IN C. ELEGANS AT ROOM TEMPERATURE?

December 2021

Heat-shocking c. elegans will translocate the DAF-16 protein into the nucleus. With translocated DAF-16 the worms will express stronger stress resistance and longevity, which we will test to see if this translocation helps c. elegans’s neurons resist traumatic injury.

Introduction: Research

SCIENTIFIC RATIONALE

HEAT SHOCK AND TBI

If heat shock protects proteins through translocation into the nucleus, than heat shock should act as a ‘protective helmet’ for worms when exposed to mechanical damage causing TBI.
The upregulation of stress response genes from DAF-16 translocation should also act as a ‘protective helmet’ for the worms exposed to mechanical damage.

HEAT SHOCK

Heat shock induces protein translocation from the cytoplasm to the nucleus (protein = DAF-16).
Translocation of DAF-16 results in an upregulation of stress response genes.
Upregulation of stress response genes promotes longevity.

TBI

C. elegans and humans have relatively similar axon structures that are affected in similar ways by mechanical stress.
Miansari et al., 2019
DAI (diffuse axonal injury) is a type of TBI (traumatic brain injury) characterised by axonal shearing, calcium balance disruption, and axonal swelling.
Blennow, K., Hardy, J., & Zetterberg, H. (2012)
Repeated TBI is linked to CTE (chronic traumatic encephaly) in humans which has been subjected to increased recent publicity due to CTE discovery in football players and soldiers.

Introduction: List

HYPOTHESIS

Heat shocked C. Elegans will be more resistant to TBI and show less commissural swelling when compared to TBI in C. elegans at room temperature.

Introduction: Text