Insect Metamorphosis Flashcards
Insecta
26 orders, found in all terrestrial habitats.
Major orders of insects with impacts on humans (O-CHILD)
Coleoptera (beetles), diptera (flies), hymenoptera (ants + bees), isoptera (termites), lepidoptera (butterfly) and orthoptera (crickets and roaches).
Insect anatomy
2 pairs of rudimentary wings, 3 pairs on legs, 2 antennae and compound eyes, CNS runs ventrally along with a respiratory tract.
Insect endocrine organs
Neurosecretory cells (lateral and medial), corpus cardiacum, corpus allatum and subesophageal ganglion.
What are endocrine organs linked to?
Metamorphosis.
How are endocrine organs linked to eyes?
Through optic lobes,
Neurosecretory cells
Secrete hormones into brain like the hypothalamus.
Corpus allatum
Secretes juvenile hormone.
Corpus cardiacum
Relay between corpus allatum and neurosecretory cells.
Why did insects evolve wings?
To escape new predators and disperse to new habitats.
Reasons for insect diversity (EDA)
Evolution of wings, diversification of mouth parts for feeding on plants and adaptive radiation of plants and insects.
Types of insect development (HAH)
Ametabolous, hemimetabolous and holometabolous.
Ametabolous development
Young resemble a small adult.
Hemimetabolous development
Incomplete metamorphosis with some structural change from youth to mature adult.
Holometabolous development (Whole)
Complete metamorphosis.
Tobacco Hornworm lifecycle
Lasts as an egg for 3-5 days then becomes a small larva (0.03g) for 6-9 days then becomes a medium larva (5g) after 4 days before a large larva (10g), then 5 days it becomes a pupa and then is an adult.
SIlkworm lifecycle
Egg, larvae, cocoon then adult moth, requires human assistance as they are domesticated.
Drosophila melanogaster (fruit fly)- life cycle
Female + Male
-> embryo
->1st instar larva
->2nd instar larva
->3rd instar larva
->prepupa
->pupa
->then hatches
Imaginal discs
Small sacs of epithelial present in the larva of drosophila and other insects, which at metamorphosis gives rise to adult structures such as wings, legs, antennae, eyes, and genitalia.
Where did metamorphosis originate?
Coleoptera and Hemiptera in the carboniferous age.
Kopec gypsy moth ligation
Got a caterpillar ligated in last larval instar, early ligated was put into one caterpillar which caused only the anterior part to pupate while if late in instar, both parts pupate.
How does the signal for pupation travel?
Anterior to posterior with a similar critical period for dependence of metamorphosis on brain.
Wigglesworth Rhodnius transplant
First instar larva glued to head of fifth instar larva, if expose body of first instar to head of 5th, then adult molt is produced but if transplant tissue such as corpus allatum from 4th to 5th you get a 6th instar stage.
What determines quality of molt?
Corpus allatum.
What inhibits metamorphosis?
Juvenile hormone.
Corpus allatum location
Always close to corpus cardiacum.
Prothoracic gland
Produces ecdysone.
Hachlow (1931)
Lepidopteran metamorphosis requires thorax tissue.
Fukuda (1940)
Prothoracic gland required in Bombyx (genus of moth) metamorphosis.
Williams (1952)
Anterior pupa with brain and prothoracic glands triggers metamorphosis posteriorly in a chain of connected pupa with no organs.
General endocrine model of metamorphosis
- PTTH from the brain is released by the CC
- PTTH stimulates the prothoracic gland to produce Ecdysone
- E is released periodically during molting
- JH from the CA determines the type of molt
PTTH
Prothoracicotropic hormone acts on prothoracic glands to regulate ecdysteroid synthesis, it has a 224AA precursor and a 109AA functional protein.
When can the pupa form?
When juvenile hormone is low and ecdysone is high.
When is PTTH released?
Triggered by environmental stimuli such as photoperiod and temperature, nervous stimuli like stretch receptors via haemolymph in bombyx and manduca or direct gland innervation in drosophila.
PTTH mode of action
Triggering a signal cascade
Via Receptor Tyrosine Kinase> Ras>Raf>ERK (in Drosophila)
Ecdysone function
Triggers transcriptional factors and programs, stimulates these to allow metamorphosis, if unchecked would form an adult molt.
Rhodnius ecdysone rhythms
Lateral clock cells and light affect PTTH neurons triggering release of PTTH that along with light influence the prothoracic gland producing ecdysone
- Binds with cyclic ecdysone receptor in target tissues
- Gene expression cascade
- Synchronisation of internal and external development cues
(See Quizlet Image)
Cyclic ecdysone receptor activation results in
Causes gene expression cascade leading to synchronisation of internal and external developmental cues.
Drosophila timekeeping cells
Keep sleep rhythm constant and excrete SNPF to PTTH neurons releasing this onto prothoracic glands.
Insulin-like peptides (ILPs)
Released from neurosecretory cells and Act beta.
Activins
Activate TGF-beta pathway.
TGF-beta pathway
Leads to Smad phosphorylation and dimerisation, then binds Medea, this activates Halloween genes.
MAPK pathway
PTTH binds receptor, ERK activates halloween genes and inhibits DHR4 prevent activation of Cyp6t3.
Insulin pathway
ILPs bind, Medea and BR phosphorylate receptor, allowing for PI3K to activate AKT activating halloween genes.
BR complex function
Provide feedback from ecdysone to ecysonal synthesis based on circulatory levels, determining molt quality.
Shade enzyme
Converts ecdysone into 20-OH Ecdysone, activating it.
Blood ecdysone
Inactivated.
How do insects acquire cholesterol?
Cannot synthesise it so require it in diet.
Ecdysteroid precursors
Sterols.
Primary site of ecdysteroid synthesis
Prothoracic gland.
Common ecdysteroids
20,26-dihydroxyecdysone and 26-OH ecdysone (embryos) and makisterone A (honeybee, hemipterans and dipterans).
Drosophila ecdysone release
Peaks at certain developmental points.
Critical development points in drosophila
Critical weight, glue gene induction, wandering, pupariation (large peak at day 5) and head eversion.
Ecdysteroid mode of action
20E binds receptor, activating it causing early Puff gene activation, that negatively feeds back on self while also activating late puff genes that were initially inhibited by 20E.
Early puff function
Act on hormone directly.
Late puff function
Secondary regulation.
What if puff pattern linked to?
Development stage.
Ultraspiracle gene
Forms a complex with ecdysone receptor gene forming early genes that form products that will inhibit the genes and activate late genes.
Key early gene product
BR-C which causes metamorphosis of salivary gland by triggering late gene expression (such as 71-E).
What inhibits BR-C?
Juvenile Hormone
What does NO act on in pre-pupa?
E75H, inhibiting it.
Prothoracic gland degeneration
Upon exposure to ecdysteroids in absence of juvenile hormone, this alone can cause apoptosis.
Where does the PG not get degenerated?
In ametabolous insects.
Juvenile hormone
It is synthesised in and released from corpus allatum, it is a lipophilic sesquiterpene and is involved in metamorphosis, diapause, reproduction and metabolism.
Most common type of Juvenile hormone
JH 3.
Hydroxy juvenile hormones
Produced in locusts and cockroaches and has greater metabolic activity.
What can JH analogs be used for?
Insecticides as they prevent sexual maturity.
JH analog insecticides
Methoprene, kinoprene and retinoic acid.
What regulates haemolymph JH titers?
Biosynthesis and degradation.
What controls JH synthesis?
Environmental stimuli (photoperiod etc.) and endogenous factors (e.g. mating and nutritional state).
Neuropeptides that affect corpus allatum activity
Allatotropins (stimulate JH production), allatostatins (inhibit JH synthesis) and allatoinhibin (inhibits Manduca corpus allatum non-reversibly).
Ovaries influence on corpus allatum
Stimulatory.
How is JH transported in haemolymph?
Bound to other molecules by JHBPs.
What can binding protect JH from?
Degradation by nonspecific tissue-bound esterases.
Juvenile hormone binding proteins
Low molecular weight binding proteins are 32kDa with 1 binding site and high molecular weight binding proteins have multiple sites.
Examples of high molecular weight binding proteins
250 and 80 kDa apoprotein and a 566kDa hexameric protein with 6 binding sites.
How is JH broken down?
Can be broken down into JH acid (JH esterase) or JH diol (JH epoxide hydrolase) and then both break down into JH acid diol by the enzyme not broken down initially.
(See Quizlet Image)
Inhibitor of precocious development in drosophila
Drosophila JH not required for prevention of precocious development, inhibition of downstream TF Broad is.
Main role of JH
Modify ecdysteroid action and prevent switch in commitment to epidermal cells, it influences stage-specific expression of genome initiated by ecdysteroids.
JH mode of action
Acts via basic helix-loop-helix PAS domain transcription factors MET and SRC.
MET
Methoprene tolerant.
SRC
Steroid receptor coactivator.
What do MET and SRC do?
They form a heterodimer which bind to JH response element in front of JH induced genes such as Kr-h1.
Kr-h1
Inhibits BROAD so larval molt forms.
What if JH isn’t present?
Met/SRC complex not formed, so no Kr-h1 which causes the larval-pupal commitment to occur.
