scholarly journals Structural Changes in Fat Body of Aedes aegypti Caused by Aging and Blood Feeding

2008 ◽  
Vol 45 (6) ◽  
pp. 1102-1107 ◽  
Author(s):  
G. F. Martins ◽  
P. F. P. Pimenta
Keyword(s):  
Aedes Aegypti ◽  
Structural Changes ◽  
Fat Body ◽  
Blood Feeding

scholarly journals Hormone-dependent activation and repression of microRNAs by the ecdysone receptor in the dengue vector mosquito Aedes aegypti

2021 ◽  
Vol 118 (26) ◽  
pp. e2102417118
Author(s):  
Ya-Zhou He ◽  
Emre Aksoy ◽  
Yike Ding ◽  
Alexander S. Raikhel
Keyword(s):  
Aedes Aegypti ◽  
Mirna Expression ◽  
Blood Meal ◽  
Fat Body ◽  
Blood Feeding ◽  
Small Rna Sequencing ◽  
Sequencing Analysis ◽  
Ecdysone Receptor ◽  
Egg Development ◽  
Semialdehyde Dehydrogenase

Female mosquitoes transmit numerous devastating human diseases because they require vertebrate blood meal for egg development. MicroRNAs (miRNAs) play critical roles across multiple reproductive processes in female Aedes aegypti mosquitoes. However, how miRNAs are controlled to coordinate their activity with the demands of mosquito reproduction remains largely unknown. We report that the ecdysone receptor (EcR)–mediated 20-hydroxyecdysone (20E) signaling regulates miRNA expression in female mosquitoes. EcR RNA-interference silencing linked to small RNA-sequencing analysis reveals that EcR not only activates but also represses miRNA expression in the female mosquito fat body, a functional analog of the vertebrate liver. EcR directly represses the expression of clustered miR-275 and miR-305 before blood feeding when the 20E titer is low, whereas it activates their expression in response to the increased 20E titer after a blood meal. Furthermore, we find that SMRTER, an insect analog of the vertebrate nuclear receptor corepressors SMRT and N-CoR, interacts with EcR in a 20E-sensitive manner and is required for EcR-mediated repression of miRNA expression in Ae. aegypti mosquitoes. In addition, we demonstrate that miR-275 and miR-305 directly target glutamate semialdehyde dehydrogenase and AAEL009899, respectively, to facilitate egg development. This study reveals a mechanism for how miRNAs are controlled by the 20E signaling pathway to coordinate their activity with the demands of mosquito reproduction.

scholarly journals The juvenile hormone receptor Methoprene-tolerant is involved in the sterilizing effect of pyriproxyfen on adult Aedes aegypti mosquitoes

2020 ◽  
Author(s):  
Tahmina Hossain Ahmed ◽  
T. Randolph Saunders ◽  
Donald Mullins ◽  
Mohammad Zillur Rahman ◽  
Jinsong Zhu
Keyword(s):  
Aedes Aegypti ◽  
Juvenile Hormone ◽  
Mosquito Control ◽  
Fat Body ◽  
Control Strategies ◽  
Follicular Development ◽  
Blood Feeding ◽  
Oocyte Development ◽  
Hormonal Responses ◽  
Before And After

AbstractExposure of adult mosquitoes to pyriproxyfen (PPF), an analog of insect juvenile hormone (JH), has shown promise to effectively sterilize female mosquitoes. However, the underlying mechanisms of the PPF-induced decrease in mosquito fecundity are largely unknown. We performed a comprehensive study to dissect the mode of PPF action in Aedes aegypti mosquitoes. Exposure to PPF prompted the overgrowth of primary follicles in sugar-fed Ae. aegypti females but blocked the development of primary follicles at Christopher’s Stage III after blood feeding. Secondary follicles were precociously activated in PPF-treated mosquitoes. Moreover, PPF substantially altered the expression of many genes that are essential for mosquito physiology and oocyte development in the fat body and ovary. In particular, many metabolic genes were differentially expressed in response to PPF treatment, thereby affecting the mobilization and utilization of energy reserves. Furthermore, PPF treatment on the previtellogenic female adults considerably modified mosquito responses to JH and 20-hydroxyecdysone (20E), two major hormones that govern mosquito reproduction. Krüppel homolog 1, a JH-inducible transcriptional regulator, showed consistently elevated expression after PPF exposure. Conversely, PPF upregulated the expression of several key players of the 20E regulatory cascades, including HR3 and E75A, in the previtellogenic stage. After blood-feeding, the expression of these 20E response genes was significantly weaker in PPF-treated mosquitoes than the solvent-treated control groups. RNAi-mediated knockdown of the Methoprene-tolerant (Met) protein, the JH receptor, partially rescued the impaired follicular development after PPF exposure and substantially increased the hatching of the eggs produced by PPF-treated female mosquitoes. Thus, the results suggested that PPF relied on Met to exert its sterilizing effects on female mosquitoes. In summary, this study finds that PPF exposure disturbs normal hormonal responses and metabolism in Ae. aegypti, shedding light on the molecular targets and the downstream signaling pathways activated by PPF.Author summaryAedes aegypti mosquitoes are responsible for the transmission of dengue, yellow fever, chikungunya, and Zika fever. Insecticides are widely used as the primary tool in the prevention and control of these infectious diseases. In light of the rapid increase of insecticide resistance in mosquito populations, there is an urgent need to find new classes of insecticides with a different mode of action. Here we found that pyriproxyfen, an analog of insect juvenile hormone (JH), had a large impact on the oocyte development, both before and after blood feeding, in female mosquitoes. Pyriproxyfen disturbed normal hormonal responses and caused metabolic shifting in female adults. These actions appear to collectively impair oocyte development and substantially reduce viable progenies of female mosquitoes. Besides, we demonstrated the involvement of the JH receptor Met in pyriproxyfen-induced female sterilization. This study significantly advances our understanding of mosquito reproductive biology and the molecular basis of pyriproxyfen action, which are invaluable for the development of new mosquito control strategies.

scholarly journals The early gene Broad is involved in the ecdysteroid hierarchy governing vitellogenesis of the mosquito Aedes aegypti

2004 ◽  
Vol 33 (3) ◽  
pp. 743-761 ◽  
Author(s):  
L Chen ◽  
J Zhu ◽  
G Sun ◽  
A S Raikhel
Keyword(s):  
Aedes Aegypti ◽  
Fat Body ◽  
Regulatory Region ◽  
Blood Feeding ◽  
Early Gene ◽  
Gene Encoding ◽  
Obvious Effect ◽  
Early Genes ◽  
Old Females

The broad (br ) gene, encoding a family of C2H2 type zinc-finger DNA-binding proteins, has been shown to act as a crucial member of the 20-hydroxyecdysone (20E) regulatory hierarchy in the fruitfly, Drosophila melanogaster and the moth, Manduca sexta. In this study, we have shown that the br gene is involved in the 20E-regulatory hierarchy controlling vitellogenesis in the mosquito, Aedes aegypti. Unlike E74 and E75 early genes, expression of br was activated in previtellogenic females, during a juvenile hormone (JH)-dependent period. The levels of Z1, Z2 and Z4 isoform mRNA were elevated in the fat body of 2-day-old females after in vitro exposure to JH III. However, JH III repressed 20E activation of br in 3-to 5-day-old females, indicating a switch in hormonal commitment. Expression of Z1, Z2 and Z4 was stimulated after blood feeding in both vitellogenic tissues, the fat body and the ovary, corresponding to peaks of ecdysteroid titers. In the fat body, the mRNA profiles of these three isoforms correlated well with those of yolk protein precursor (YPP) genes. These BR isoforms were activated by 20E in fat bodies cultured in vitro and behaved as early genes, with a self-repressive autoregulatory loop that can be blocked by the protein inhibitor, cyclohexamide. Multiple binding sites for all four BR isoforms were present in the 5′-regulatory region of the major YPP gene, vitellogenin (Vg). Effects of BR isoforms on the expression of Vg have been demonstrated by cell transfection analysis. In particular, BR isoforms by themselves had no effects on the Vg promoter. However, Z1 and Z4 each repressed Aedes aegypti ecdysone receptor (EcR)/Ultraspiracle (USP)-mediated 20E activation of the Vg promoter, while Z2 enhanced activation of the Vg promoter by AaEcR/AaUSP in the presence of 20E. Z3 had no obvious effect in the same experiment. These results suggested that BR isoforms are essential for proper activation and termination of the Vg gene in response to 20E. Overall, our study implicated br in the regulation of mosquito vitellogenesis.

scholarly journals Human blood microRNA hsa-miR-21-5p induces vitellogenin in the mosquito Aedes aegypti

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Hugo D. Perdomo ◽  
Mazhar Hussain ◽  
Rhys Parry ◽  
Kayvan Etebari ◽  
Lauren M. Hedges ◽  
...  
Keyword(s):  
Aedes Aegypti ◽  
Human Blood ◽  
Egg Production ◽  
Fat Body ◽  
Blood Feeding ◽  
Mosquito Vectors ◽  
Progeny Production ◽  
Proteomics Analysis ◽  
Gene Coding ◽  
Reproductive Events

AbstractMosquito vectors transmit various diseases through blood feeding, required for their egg development. Hence, blood feeding is a major physiological event in their life cycle, during which hundreds of genes are tightly regulated. Blood is a rich source of proteins for mosquitoes, but also contains many other molecules including microRNAs (miRNAs). Here, we found that human blood miRNAs are transported abundantly into the fat body tissue of Aedes aegypti, a key metabolic center in post-blood feeding reproductive events, where they target and regulate mosquito genes. Using an artificial diet spiked with the mimic of an abundant and stable human blood miRNA, hsa-miR-21-5p, and proteomics analysis, we found over 40 proteins showing differential expression in female Ae. aegypti mosquitoes after feeding. Of interest, we found that the miRNA positively regulates the vitellogenin gene, coding for a yolk protein produced in the mosquito fat body and then transported to the ovaries as a protein source for egg production. Inhibition of hsa-miR-21-5p followed by human blood feeding led to a statistically insignificant reduction in progeny production. The results provide another example of the involvement of small regulatory molecules in the interaction of taxonomically vastly different taxa.

scholarly journals Serotonin signaling regulates insulin-like peptides for growth, reproduction, and metabolism in the disease vector Aedes aegypti

2018 ◽  
Vol 115 (42) ◽  
pp. E9822-E9831 ◽  
Author(s):  
Lin Ling ◽  
Alexander S. Raikhel
Keyword(s):  
Body Size ◽  
Aedes Aegypti ◽  
Serotonin Receptor ◽  
Fat Body ◽  
Transcript Level ◽  
Blood Feeding ◽  
Rnai Silencing ◽  
Regulatory Link ◽  
Serotonin Signaling ◽  
Lipid Stores

Disease-transmitting female mosquitoes require a vertebrate blood meal to produce their eggs. An obligatory hematophagous lifestyle, rapid reproduction, and existence of a large number of transmittable diseases make mosquitoes the world’s deadliest animals. Attaining optimal body size and nutritional status is critical for mosquitoes to become reproductively competent and effective disease vectors. We report that blood feeding boosts serotonin concentration and elevates the serotonin receptor Aa5HT2B (Aedes aegypti 5-hydroxytryptamine receptor, type 2B) transcript level in the fat-body, an insect analog of the vertebrate liver and adipose tissue. Aa5HT2B gene disruption using the CRISPR-Cas9 gene-editing approach led to a decreased body size, postponed development, shortened lifespan, retarded ovarian growth, and dramatically diminished lipid accumulation. Expression of the insulin-like peptide (ILP) genes ilp2 and ilp6 was down-regulated while that of ilp5 and ilp4 was up-regulated in response to Aa5HT2B disruption. CRISPR-Cas9 disruption of ilp2 or ilp6 resulted in adverse phenotypes similar to those of Aa5HT2B disruption, while ilp5 CRISPR-Cas9 disruption had exactly the opposite effect on growth and metabolism, with significantly increased body size and elevated lipid stores. Simultaneous CRISPR-Cas9 disruption of Aa5HT2B and ilp5 rescued these phenotypic manifestations. Aa5HT2B RNAi silencing rendered ilp6 insensitive to serotonin treatment in the cultured fat-body, suggesting a regulatory link between Aa5HT2B and ILP6. Moreover, CRISPR-Cas9 ilp6 disruption affects expression of ilp-2, -5, and -4, pointing out on a possible role of ILP6 as a mediator of the Aa5HT2B action.

scholarly journals Aedes aegypti (Diptera: Culicidae) Immune Responses with Different Feeding Regimes Following Infection by the Entomopathogenic Fungus Metarhizium anisopliae

Insects ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 95 ◽  
Author(s):  
Sara Cabral ◽  
Adriano de Paula ◽  
Richard Samuels ◽  
Rodrigo da Fonseca ◽  
Simone Gomes ◽  
...  
Keyword(s):  
Aedes Aegypti ◽  
Immune Responses ◽  
Antimicrobial Peptides ◽  
Fungal Infection ◽  
Fat Body ◽  
Negative Regulator ◽  
Toll Pathway ◽  
Promising Alternative ◽  
Imd Pathway ◽  
Feeding Regimes

The mosquito Aedes aegypti is the most notorious vector of illness-causing viruses. The use of entomopathogenic fungi as bioinsecticides is a promising alternative for the development of novel mosquito control strategies. We investigate whether differences in immune responses could be responsible for modifications in survival rates of insects following different feeding regimes. Sucrose and blood-fed adult A. aegypti females were sprayed with M. anisopliae 1 × 106 conidia mL−1, and after 48 h, the midgut and fat body were dissected. We used RT-qPCR to monitor the expression of Cactus and REL1 (Toll pathway), IMD, REL2, and Caspar (IMD pathway), STAT and PIAS (JAK-STAT pathway), as well as the expression of antimicrobial peptides (Defensin A, Attacin and Cecropin G). REL1 and REL2 expression in both the midgut and fat body were higher in blood-fed fungus-challenged A. aegypti than in sucrose-fed counterparts. Interestingly, infection of sucrose-fed insects induced Cactus expression in the fat body, a negative regulator of the Toll pathway. The IMD gene was upregulated in the fat body in response to fungal infection after a blood meal. Additionally, we observed the induction of antimicrobial peptides in the blood-fed fungus-challenged insects. This study suggests that blood-fed A. aegypti are less susceptible to fungal infection due to the rapid induction of Toll and IMD immune pathways.

scholarly journals The Fat Body Transcriptomes of the Yellow Fever Mosquito Aedes aegypti, Pre- and Post- Blood Meal

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e22573 ◽  
Author(s):  
David P. Price ◽  
Vijayaraj Nagarajan ◽  
Alexander Churbanov ◽  
Peter Houde ◽  
Brook Milligan ◽  
...  
Keyword(s):  
Aedes Aegypti ◽  
Yellow Fever ◽  
Blood Meal ◽  
Fat Body ◽  
Yellow Fever Mosquito

scholarly journals Characterization of a vasodilator from the salivary glands of the yellow fever mosquito Aedes aegypti

1992 ◽  
Vol 165 (1) ◽  
pp. 61-71 ◽  
Author(s):  
J. M. Ribeiro
Keyword(s):  
Salivary Gland ◽  
Aedes Aegypti ◽  
Salivary Glands ◽  
Posterior Part ◽  
Aortic Ring ◽  
Blood Feeding ◽  
Reversed Phase ◽  
Relative Molecular Mass ◽  
Vasodilatory Activity ◽  
Carboxy Terminal

Salivary gland homogenates and oil-induced saliva of the mosquito Aedes aegypti dilate the rabbit aortic ring and contract the guinea pig ileum. The vasodilatory activity is endothelium-dependent, heat-stable, sensitive to both trypsin and chymotrypsin treatments, and both smooth muscle activities cross-desensitize to the tachykinin peptide substance P. Both bioactivities co-elute when salivary gland homogenates are fractionated by reversed-phase HPLC. Molecular sieving chromatography indicates a relative molecular mass of 1400. A monoclonal antibody specific to the carboxy terminal region of tachykinins reacts with material in the posterior part of the central lobe of paraformaldehyde-fixed salivary glands. The presence of a vasodilatory peptide of the tachykinin family in the salivary glands of A. aegypti is proposed and its role in blood feeding is discussed.

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