Lecture 5: Sterile Insect Technique and other forms of control

What is the Sterile Insect Technique (SIT)?

A biological control method in which large numbers of sterile male insects are released to compete with wild males for mates; females that mate with sterile males produce no offspring.

What is the goal of SIT?

To suppress or eradicate pest populations by reducing successful reproduction in the wild.

Why do sterile males not persist in the environment?

They are non-reproducing, so their numbers decline naturally; they cannot establish a self-sustaining population.

What are the basic principles of SIT?

Release treated sterile males in large numbers; females mate only once; sterile matings yield no viable offspring; population or pathogen transmission declines.

Why does SIT work best when females mate once?

Because one sterile mating permanently removes a female from the reproductive pool, maximizing population reduction.

How are males made sterile for SIT?

By irradiation (X-rays, gamma rays), genetic manipulation (RIDL), or Wolbachia infection causing cytoplasmic incompatibility.

What is RIDL?

“Release of Insects carrying a Dominant Lethal” gene—a genetic control strategy where released insects carry a lethal gene that kills their offspring.

How does RIDL work in practice?

In lab, the lethal gene is repressed with tetracycline (so they survive); in the wild, absence of tetracycline activates the gene, causing offspring death.

What is the molecular system behind RIDL?

tTAV (tetracycline-repressible transcriptional activator) drives over-expression of itself when tetracycline is absent, which is toxic; fluorescence markers identify GM insects.

What is the marker gene used for in RIDL insects?

It allows researchers to track released GM mosquitoes and their progeny using fluorescence in the eyes.

What are advantages of RIDL?

Species-specific, self-limiting, environmentally friendly, and can precisely target vector populations such as Aedes aegypti.

What is Wolbachia?

An intracellular Gram-negative bacterium (Order Rickettsiales) infecting arthropods and nematodes; maternally transmitted through eggs.

What types of Wolbachia–host relationships exist?

They range from parasitic (male killing, feminization) to mutualistic (nutrient provisioning, immune evasion).

What reproductive manipulations can Wolbachia cause?

Male killing, feminization, parthenogenesis, and cytoplasmic incompatibility.

What is cytoplasmic incompatibility (CI)?

A reproductive barrier where infected males and uninfected females produce inviable offspring; infected females transmit Wolbachia to all offspring.

How does Wolbachia spread through a mosquito population?

Infected females produce infected offspring regardless of mate type; infection spreads quickly by maternal transmission.

How does Wolbachia help control diseases like dengue?

It interferes with virus replication inside mosquitoes, reducing their ability to transmit dengue, Zika, and other arboviruses.

What lab steps are taken to use Wolbachia for vector control?

Create stable Wolbachia-infected Aedes aegypti lines; verify viral suppression; test safety; monitor spread and effectiveness in wild populations.

What is the significance of Wolbachia’s cytoplasmic incompatibility for SIT-like programs?

It mimics sterility—infected males mating with uninfected females yield no viable offspring, suppressing mosquito populations.

What was the first successful SIT program?

The eradication of the New World screwworm (Cochliomyia hominivorax) in the 1950s using irradiated sterile males.

What maintains screwworm eradication today?

A sterile-male buffer zone at the Darién Gap between Panama and Colombia prevents reintroduction.

How does Wolbachia infection differ from RIDL?

Wolbachia uses natural bacterial symbiosis to induce sterility or pathogen blocking; RIDL uses engineered lethal genes controlled by tetracycline.

What is parthenogenesis caused by Wolbachia?

Reproduction by infected females without fertilization—offspring develop from unfertilized eggs.

What is male killing in Wolbachia infections?

Infected male larvae die early, biasing the sex ratio toward transmitting females.

What is feminization caused by Wolbachia?

Infected genetic males develop as functional females or infertile pseudo-females.

What is mutualism in Wolbachia–host relations?

Bacterium provides benefits such as nutrient provisioning or virus protection, improving host survival or fecundity.

How does SIT compare with pesticide use?

SIT suppresses populations biologically without chemical residues or broad ecological harm, unlike conventional pesticides.

What is the neuron’s structure shown in the pesticide slide?

Dendrites receive impulses, soma integrates, axon carries signals away, and axon terminals transmit to other neurons or muscles.

How do insecticides exploit insect neurons?

They target neurotransmission processes (acetylcholine cycle or sodium channel conduction) to cause paralysis and death.

How does acetylcholine (ACh) normally function?

Released at synapse, binds to ACh receptors on the next neuron or muscle, then is broken down by acetylcholinesterase (AChE) to stop the signal.

How do organophosphate (OP) insecticides act?

They inhibit AChE, causing ACh buildup and continuous nerve stimulation leading to tremors, convulsions, paralysis, and death.

How do neonicotinoid insecticides act?

They mimic ACh (agonists at ACh receptors) but are not degraded by AChE, resulting in persistent activation and paralysis.

How do pyrethroid insecticides act?

They keep sodium channels open longer, causing repetitive nerve firing and depolarization, leading to tremors and incoordination.

What are typical symptoms of pyrethroid poisoning in insects?

Tremors, convulsions, salivation, uncoordinated movement, and death.

What are main target sites of neurotoxic insecticides?

Acetylcholinesterase (AChE), acetylcholine receptors, and voltage-gated sodium channels.

Why do insecticides often also affect humans?

Insects and humans share similar neuron structures and neurotransmitter systems, though insecticides are designed to be more selective for insect receptors.

What causes insecticide resistance?

Genetic changes in pest populations that reduce insecticide effectiveness after repeated exposure (selection pressure).

How does resistance evolve in a population?

Susceptible insects die; resistant individuals survive and pass resistance genes to offspring; over generations the population becomes resistant.

What factors accelerate resistance development?

Short generation time, high fecundity, dominance of resistance alleles, strong selection pressure, and gene flow bringing in resistant alleles.

What factors slow resistance development?

Long generation time, low fecundity, fitness costs of resistance, multiple-gene (polygenic) control, and limited gene flow.

What is selection pressure?

The intensity of insecticide use that favors survival of resistant genotypes over susceptible ones.

What is IRM (Insecticide Resistance Management)?

Strategies like rotating insecticide classes, using biological control, and integrating methods to delay resistance.

What is the outcome of unchecked resistance?

A resistant population dominates and insecticide control fails, leading to renewed disease transmission or crop damage.

How does SIT help avoid resistance problems?

It does not rely on chemical toxicity; population suppression through sterility avoids selecting for detoxification or target-site mutations.