Figure 1.

Possible impacts of epithelial dynamics in the mosquito midgut on the hematophagous lifecycle, aging, interactions with gut flora, Plasmodium and arboviral infections. (A) During the post-emergence maturation, JH could stimulate ISCs to proliferate and create new ECs or prompt ECs to endocycle to attain higher ploidy; blood-feeding stimulates the production of 20E, which could stimulate the proliferation of ISCs, the differentiation of new ECs, and transcriptional changes in ECs. (B) Normal microbiota could contribute to aging and basal turnover of EC populations; dying ECs could stimulate ISCs to effect homeostatic replacement; dysbiosis and/or infection with oral bacterial pathogens could accelerate the turnover of epithelial cells; ISC-mediated repair could serve as a disease tolerance mechanism, promoting mosquito survival. Invasion by Plasmodium (C) and/or arboviral pathogens (D) could prompt cell sacrifice mechanisms to limit pathogenic success; ISC proliferation and differentiation could help infected mosquitoes to tolerate epithelial damage.