As the most important vectors of malaria, sympathy for female Anopheles gambiae mosquitoes is understandably in short supply, but they live very stressful lives. They risk infection with Plasmodium parasites when they feed and are exposed to dramatic diurnal temperature changes. In a paper published in Communications Biology by our group, together with colleagues at Harvard University, Boston, USA, reveals how mosquitoes balance the need to stay alive (by fighting infection or resisting heat stress), with the need to reproduce (by investing in egg production).  The mechanism they uncover involves the modification of steroid hormone production under stress conditions. Interestingly, this is reminiscent of the situation found in women suffering from polyendocrine metabolic ovarian syndrome (PMOS), highlighting the universal nature of the problem of balancing stress and reproduction. It is hoped that better understanding of how this balancing act is maintained in mosquitoes may yield opportunities to intervene to reduce their numbers and shorten their lives, so limiting their ability to transmit malaria-causing parasites. 

You can find the research article here.

In addition, Matthew has written an accompanying blog post in Springer Nature Research Communities, Behind the Paper "Life, Death, and Egg Counting: How Mosquitoes Prioritize Survival Over Reproduction" that can be found at this link.

Abstract
Environmental stress can limit mammalian reproduction by affecting production of sexual steroid hormones. Here we reveal a similar mechanism in the malarial mosquito Anopheles gambiae: activation of the stress-sensitive c-Jun N-terminal kinase, JNK, constrains reproductive investment by suppressing production of ecdysteroids that orchestrate egg development in this species. We show that infection with Plasmodium berghei (P. berghei) parasites increases JNK signalling in the reproductive tract causing a JNK-dependent reduction in both egg development and mosquito survival. Moreover, JNK signaling suppresses expression of a rate-limiting enzyme in ecdysteroid synthesis, Cyp315a1 (AGAP000284), a transcriptional change reflected in reduced ecdysteroid production following an infected blood meal. We demonstrate experimentally that a similar mechanism limits egg production under other stressors (heat stress, or ectopic activation of JNK signaling). Together, these data connect stress-induced JNK activation to Cyp315a1 suppression and reduced ecdysteroid levels in a regulatory circuit by which P. berghei infection curtails reproductive investment in an important vector of human malaria, a mechanism that may be applicable to environmental stressors more generally.