ABSTRACT
The Nuneztovari Complex of Anopheles (Diptera: Culicidae) comprises four species: An. nuneztovari Gabaldon, An. goeldii Rozeboom Gabaldon, An. dunhami Causey and An. nuneztovari species A. This study aimed to identify morphologically the species of the Nuneztovari Complex that occur in the area of the Belo Monte hydroelectric dam. The morphological identification of adult males and male genitalia (aedeagus and ventral claspette) was performed. A statistical analysis of the difference in aedeagal leaflet length was done using the Mann-Whitney test. Of the 38 male genitalia of specimens of the Nuneztovari Complex examined, 33 were identified as An. goeldii/An. nuneztovari A and five as An. nuneztovari s.s. A statistically significant difference in aedeagal leaflet length was detected between the species: the mean length was 1.23 µm for An. goeldii/An. nuneztovari A and 9.18 µm for An. nuneztovari s.s. This is the first record of An. nuneztovari s.s.in areas of environmental modification in the Brazilian Amazon. This study provides a measurement tool that can identify and differentiate species of the complex in the region, which can be applied to the other species of the complex as well to other anopheline species; thus, fostering the acquisition of information about the role of each species in malaria transmission.
Subject(s)
Anopheles , Malaria , Animals , Brazil , Genitalia, Male , MaleABSTRACT
The male-biased prevalence of certain neurodevelopmental disorders and the sex-biased outcomes associated with stress exposure during gestation have been previously described. Here, we hypothesized that genes distinctively targeted by only one or both homologous proteins highly conserved across therian mammals, SOX3 and SRY, could induce sexual adaptive changes that result in a differential risk for neurodevelopmental disorders. ChIP-seq/chip data showed that SOX3/SRY gene targets were expressed in different brain cell types in mice. We used orthologous human genes in rodent genomes to extend the number of SOX3/SRY set (1,721). These genes were later found to be enriched in five modules of coexpressed genes during the early and mid-gestation periods (FDR < 0.05), independent of sexual hormones. Genes with differential expression (24, p < 0.0001) and methylation (40, p < 0.047) between sexes were overrepresented in this set. Exclusive SOX3 or SRY target genes were more associated with the late gestational and postnatal periods. Using autism as a model sex-biased disorder, the SOX3/SRY set was enriched in autism gene databases (FDR ≤ 0.05), and there were more de novo variations from the male autism spectrum disorder (ASD) samples under the SRY peaks compared to the random peaks (p < 0.024). The comparison of coexpressed networks of SOX3/SRY target genes between male autism and control samples revealed low preservation in gene modules related to stress response (99 genes) and neurogenesis (78 genes). This study provides evidence that while SOX3 is a regulatory mechanism for both sexes, the male-exclusive SRY also plays a role in gene regulation, suggesting a potential mechanism for sex bias in ASD.