Insect Metamorphosis Flashcards

1
Q

Insecta

A

26 orders, found in all terrestrial habitats.

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2
Q

Major orders of insects with impacts on humans (O-CHILD)

A

Coleoptera (beetles), diptera (flies), hymenoptera (ants + bees), isoptera (termites), lepidoptera (butterfly) and orthoptera (crickets and roaches).

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3
Q

Insect anatomy

A

2 pairs of rudimentary wings, 3 pairs on legs, 2 antennae and compound eyes, CNS runs ventrally along with a respiratory tract.

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4
Q

Insect endocrine organs

A

Neurosecretory cells (lateral and medial), corpus cardiacum, corpus allatum and subesophageal ganglion.

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5
Q

What are endocrine organs linked to?

A

Metamorphosis.

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6
Q

How are endocrine organs linked to eyes?

A

Through optic lobes,

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7
Q

Neurosecretory cells

A

Secrete hormones into brain like the hypothalamus.

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8
Q

Corpus allatum

A

Secretes juvenile hormone.

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9
Q

Corpus cardiacum

A

Relay between corpus allatum and neurosecretory cells.

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10
Q

Why did insects evolve wings?

A

To escape new predators and disperse to new habitats.

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11
Q

Reasons for insect diversity (EDA)

A

Evolution of wings, diversification of mouth parts for feeding on plants and adaptive radiation of plants and insects.

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12
Q

Types of insect development (HAH)

A

Ametabolous, hemimetabolous and holometabolous.

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13
Q

Ametabolous development

A

Young resemble a small adult.

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14
Q

Hemimetabolous development

A

Incomplete metamorphosis with some structural change from youth to mature adult.

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15
Q

Holometabolous development (Whole)

A

Complete metamorphosis.

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16
Q

Tobacco Hornworm lifecycle

A

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.

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17
Q

SIlkworm lifecycle

A

Egg, larvae, cocoon then adult moth, requires human assistance as they are domesticated.

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18
Q

Drosophila melanogaster (fruit fly)- life cycle

A

Female + Male
-> embryo
->1st instar larva
->2nd instar larva
->3rd instar larva
->prepupa
->pupa
->then hatches

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19
Q

Imaginal discs

A

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.

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20
Q

Where did metamorphosis originate?

A

Coleoptera and Hemiptera in the carboniferous age.

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21
Q

Kopec gypsy moth ligation

A

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.

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22
Q

How does the signal for pupation travel?

A

Anterior to posterior with a similar critical period for dependence of metamorphosis on brain.

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23
Q

Wigglesworth Rhodnius transplant

A

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.

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24
Q

What determines quality of molt?

A

Corpus allatum.

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25
Q

What inhibits metamorphosis?

A

Juvenile hormone.

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26
Q

Corpus allatum location

A

Always close to corpus cardiacum.

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27
Q

Prothoracic gland

A

Produces ecdysone.

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28
Q

Hachlow (1931)

A

Lepidopteran metamorphosis requires thorax tissue.

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29
Q

Fukuda (1940)

A

Prothoracic gland required in Bombyx (genus of moth) metamorphosis.

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30
Q

Williams (1952)

A

Anterior pupa with brain and prothoracic glands triggers metamorphosis posteriorly in a chain of connected pupa with no organs.

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31
Q

General endocrine model of metamorphosis

A
  • 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
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32
Q

PTTH

A

Prothoracicotropic hormone acts on prothoracic glands to regulate ecdysteroid synthesis, it has a 224AA precursor and a 109AA functional protein.

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33
Q

When can the pupa form?

A

When juvenile hormone is low and ecdysone is high.

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34
Q

When is PTTH released?

A

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.

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35
Q

PTTH mode of action

A

Triggering a signal cascade

Via Receptor Tyrosine Kinase> Ras>Raf>ERK (in Drosophila)

36
Q

Ecdysone function

A

Triggers transcriptional factors and programs, stimulates these to allow metamorphosis, if unchecked would form an adult molt.

37
Q

Rhodnius ecdysone rhythms

A

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)

38
Q

Cyclic ecdysone receptor activation results in

A

Causes gene expression cascade leading to synchronisation of internal and external developmental cues.

39
Q

Drosophila timekeeping cells

A

Keep sleep rhythm constant and excrete SNPF to PTTH neurons releasing this onto prothoracic glands.

40
Q

Insulin-like peptides (ILPs)

A

Released from neurosecretory cells and Act beta.

41
Q

Activins

A

Activate TGF-beta pathway.

42
Q

TGF-beta pathway

A

Leads to Smad phosphorylation and dimerisation, then binds Medea, this activates Halloween genes.

43
Q

MAPK pathway

A

PTTH binds receptor, ERK activates halloween genes and inhibits DHR4 prevent activation of Cyp6t3.

44
Q

Insulin pathway

A

ILPs bind, Medea and BR phosphorylate receptor, allowing for PI3K to activate AKT activating halloween genes.

45
Q

BR complex function

A

Provide feedback from ecdysone to ecysonal synthesis based on circulatory levels, determining molt quality.

46
Q

Shade enzyme

A

Converts ecdysone into 20-OH Ecdysone, activating it.

47
Q

Blood ecdysone

A

Inactivated.

48
Q

How do insects acquire cholesterol?

A

Cannot synthesise it so require it in diet.

49
Q

Ecdysteroid precursors

A

Sterols.

50
Q

Primary site of ecdysteroid synthesis

A

Prothoracic gland.

51
Q

Common ecdysteroids

A

20,26-dihydroxyecdysone and 26-OH ecdysone (embryos) and makisterone A (honeybee, hemipterans and dipterans).

52
Q

Drosophila ecdysone release

A

Peaks at certain developmental points.

53
Q

Critical development points in drosophila

A

Critical weight, glue gene induction, wandering, pupariation (large peak at day 5) and head eversion.

54
Q

Ecdysteroid mode of action

A

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.

55
Q

Early puff function

A

Act on hormone directly.

56
Q

Late puff function

A

Secondary regulation.

57
Q

What if puff pattern linked to?

A

Development stage.

58
Q

Ultraspiracle gene

A

Forms a complex with ecdysone receptor gene forming early genes that form products that will inhibit the genes and activate late genes.

59
Q

Key early gene product

A

BR-C which causes metamorphosis of salivary gland by triggering late gene expression (such as 71-E).

60
Q

What inhibits BR-C?

A

Juvenile Hormone

61
Q

What does NO act on in pre-pupa?

A

E75H, inhibiting it.

62
Q

Prothoracic gland degeneration

A

Upon exposure to ecdysteroids in absence of juvenile hormone, this alone can cause apoptosis.

63
Q

Where does the PG not get degenerated?

A

In ametabolous insects.

64
Q

Juvenile hormone

A

It is synthesised in and released from corpus allatum, it is a lipophilic sesquiterpene and is involved in metamorphosis, diapause, reproduction and metabolism.

65
Q

Most common type of Juvenile hormone

A

JH 3.

66
Q

Hydroxy juvenile hormones

A

Produced in locusts and cockroaches and has greater metabolic activity.

67
Q

What can JH analogs be used for?

A

Insecticides as they prevent sexual maturity.

68
Q

JH analog insecticides

A

Methoprene, kinoprene and retinoic acid.

69
Q

What regulates haemolymph JH titers?

A

Biosynthesis and degradation.

70
Q

What controls JH synthesis?

A

Environmental stimuli (photoperiod etc.) and endogenous factors (e.g. mating and nutritional state).

71
Q

Neuropeptides that affect corpus allatum activity

A

Allatotropins (stimulate JH production), allatostatins (inhibit JH synthesis) and allatoinhibin (inhibits Manduca corpus allatum non-reversibly).

72
Q

Ovaries influence on corpus allatum

A

Stimulatory.

73
Q

How is JH transported in haemolymph?

A

Bound to other molecules by JHBPs.

74
Q

What can binding protect JH from?

A

Degradation by nonspecific tissue-bound esterases.

75
Q

Juvenile hormone binding proteins

A

Low molecular weight binding proteins are 32kDa with 1 binding site and high molecular weight binding proteins have multiple sites.

76
Q

Examples of high molecular weight binding proteins

A

250 and 80 kDa apoprotein and a 566kDa hexameric protein with 6 binding sites.

77
Q

How is JH broken down?

A

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)

78
Q

Inhibitor of precocious development in drosophila

A

Drosophila JH not required for prevention of precocious development, inhibition of downstream TF Broad is.

79
Q

Main role of JH

A

Modify ecdysteroid action and prevent switch in commitment to epidermal cells, it influences stage-specific expression of genome initiated by ecdysteroids.

80
Q

JH mode of action

A

Acts via basic helix-loop-helix PAS domain transcription factors MET and SRC.

81
Q

MET

A

Methoprene tolerant.

82
Q

SRC

A

Steroid receptor coactivator.

83
Q

What do MET and SRC do?

A

They form a heterodimer which bind to JH response element in front of JH induced genes such as Kr-h1.

84
Q

Kr-h1

A

Inhibits BROAD so larval molt forms.

85
Q

What if JH isn’t present?

A

Met/SRC complex not formed, so no Kr-h1 which causes the larval-pupal commitment to occur.