Stress-induced reproductive arrest in Drosophila occurs through ETH deficiency-mediated suppression of oogenesis and ovulation

Autor: Timothy G. Kingan, Matthew Meiselman, Michael E. Adams
Rok vydání: 2017
Předmět:
0301 basic medicine
Physiology
medicine.medical_treatment
Plant Science
Molting
Oogenesis
chemistry.chemical_compound
0302 clinical medicine
Structural Biology
2.1 Biological and endogenous factors
Aetiology
lcsh:QH301-705.5
media_common
Neurons
Reproduction
Biological Sciences
Juvenile Hormones
Drosophila melanogaster
Ecdysis
Insect Hormones
Oviduct
Female
General Agricultural and Biological Sciences
Endocrine
Ecdysone
Heat and nutrient stress
Biotechnology
Research Article
Ovulation
medicine.medical_specialty
Physiological
media_common.quotation_subject
Biology
Stress
General Biochemistry
Genetics and Molecular Biology
03 medical and health sciences
Stress
Physiological
Internal medicine
medicine
Ecdysis triggering hormone
Animals
Octopamine
Ecology
Evolution
Behavior and Systematics
Liberin
Contraception/Reproduction
Cell Biology
Steroid hormone
030104 developmental biology
Endocrinology
lcsh:Biology (General)
chemistry
Juvenile hormone
030217 neurology & neurosurgery
Developmental Biology
Hormone
Zdroj: BMC Biology
BMC Biology, Vol 16, Iss 1, Pp 1-15 (2018)
BMC biology, vol 16, iss 1
ISSN: 1741-7007
Popis: Background Environmental stressors induce changes in endocrine state, leading to energy re-allocation from reproduction to survival. Female Drosophila melanogaster respond to thermal and nutrient stressors by arresting egg production through elevation of the steroid hormone ecdysone. However, the mechanisms through which this reproductive arrest occurs are not well understood. Results Here we report that stress-induced elevation of ecdysone is accompanied by decreased levels of ecdysis triggering hormone (ETH). Depressed levels of circulating ETH lead to attenuated activity of its targets, including juvenile hormone-producing corpus allatum and, as we describe here for the first time, octopaminergic neurons of the oviduct. Elevation of steroid thereby results in arrested oogenesis, reduced octopaminergic input to the reproductive tract, and consequent suppression of ovulation. ETH mitigates heat or nutritional stress-induced attenuation of fecundity, which suggests that its deficiency is critical to reproductive adaptability. Conclusions Our findings indicate that, as a dual regulator of octopamine and juvenile hormone release, ETH provides a link between stress-induced elevation of ecdysone levels and consequent reduction in fecundity. Electronic supplementary material The online version of this article (10.1186/s12915-018-0484-9) contains supplementary material, which is available to authorized users.
Databáze: OpenAIRE
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