Evolution of Semelparity

Question 1

Describe the features of antechinus reproductive biology

Answer 1

• Small carnivorous marsupial
• Habitat – forests of south eastern Australia
• Males exhibit semelparity → single reproductive episode before death.
− Iteroparity is multiple reproductive cycles over the course of a lifetime.
• Breeding is incredibly seasonal – restricted to just a few months of the year.

Sperm Production
• Total spermatogenic failure occurs 1 month before the breeding season
• Epididymis has limited capacity for sperm storage
• Very few sperm remain in the tract at the end of the breeding season

Reproduction
• Females can store sperm in specialised crypts in the oviduct for up to 2 weeks
• Genetic studies show multiple paternity within one litter, indicating that sperm from several males may be stored
• In the wild, a lecking system has been proposed – males congregate at specialised mating areas
• There is intense male-male competition for access to females.

Male die off following mating:
• After each reproductive event, all males die off
− Copulation lasts 8-12 hours
− Towards the end of the breeding season, males are in awful condition with fur loss and body weight loss.
• Males die off before the offspring have left the nest
• The population runs off the females and her offspring
− The pouched young are the smallest mammals – they weight only 16mg
− After weaning, the young males rapidly leave the maternal area
• This is the shortest lived mammal on the planet

Question 2

What do the male antechinuses die of?

Answer 2

• Haemorhagic ulcerations of the gastric mucosa, blood in lower intestines
• Increased invasiveness of parasites and micro-organisms
• Commonly, invasion of lung by nematode worm parasites
• All associated with collapse of immune system
• All are symptoms of persistent stress and inflammation in response to GCs!

Question 3

What is the stress hypothesis of male die off in the antechinus?

Answer 3

HPA axis:
• CRH released from hippocampus
• Acts on anterior pituitary to release ACTH
• Acts on adrenal cortex to release GCs
• Corticosteroid binding globulins can bind to corticosteroids – making them less available at the target.
• CBG index tells us how much free cortisol there is.

Seasonal changes in CBG binding in males
• Before the breeding season, the ratio is around 70%
• As you progress through the season, the proportion of bound cortisol drops dramatically → increases proportion of free corticosteroids.
• These changes don’t occur in females → so something in the males is changing the biology of action of GCs.

Relationship with Testosterone
• The drop in CBG through the mating system is correlated with a rise in testosterone
• CBG is a steroid-dependent target – regulated by sex steroids – rise in testosterone brings about the drop in CBG
• Males have peak testosterone levels at die off – so they will also have peak free cortisol

Question 4

What is the mechanism by which stress leads to semelparity?

Answer 4

Biology of GCs:
• GCs are carbs – they cause hyperglycaemia
• Deficiency gives low glucose and low liver glycogen
• GCs stimulate gluconeogenesis, decrease glucose oxidation and cause insulin resistance
• They also suppress the immune and inflammatory systems!
• → Trade off between benefit of increased GCs and cost of reduced immune system

Seasonal Collapse of Feedback
• Elevated testosterone reduces the activity of binding globulins
• Negative feedback appears to be disabled

Testing the feedback:
• Use dexamethasone – synthetic corticosteroid

Before the breeding season:
• If we administer DEX, this activates the GR in the hippocampus giving negative feedback
• This leads to a repression of CRH, reduced ACTH and then lowered cortisol
• → this is the classic effect of corticosteroids in the brain.

• If we add ACTH into the male antechinus, this stimulates the adrenal cortex and leads to an increase in cortisol
• → So, before the breeding season, you can drive the male HPA axis in the perfectly normal way

During the breeding season:
• You can still drive the adrenal cortex by administering ACTH → indication that the pituitary gland and ACTH is not the primary mechanism involves in this seasonal stress response
• However, if you administer DEX, there is now no cortisol response → you have lost the negative feedback

So:
• Brain (likely hippocampal) GR negative feedback system is shut down during the feedback season
• This is activated by seasonally rising testosterone - brings about the drop in CBGs
• Failure of GR feedback leads to metabolic collapse and deathl