No abstract

Seasonal variation of color patterns on butterfly wings are iconic examples of developmentally plastic traits that can influence adaptation and speciation. Yet, there are few examples of such seasonal polyphenisms that have characterized the environmental cues, ecological consequences, or genetic mechanisms involved in generating the plastic variation of wing color. Further, there is a lack of support that such plasticity may impact the adaptive diversification of butterfly wing patterns. Here, we report a case of seasonal polyphenism in pigment and structurally-based color patterns of Zerene cesonia that are strikingly similar to the color pattern divergence seen on the wings of sulphur butterflies. We show that (i) coordinated changes in temperature and photoperiod drive the plasticity, (ii) the plastic color changes impact how fast the butterflies can warm, (iii) identify spalt as likely be involved the genetic coupling of the pigment and structurally-based color plastic response. We further show that this plastic wing changes phenocopy wing pattern divergence between Zerene species, as well as the color pattern differences known to be commonly involved in sexual selection and speciation across sulphur butterflies. Together, our results demonstrate that shared environmental cues and genetic basis for pigment and structural color plasticity may result in conditions that may have facilitated species diversification of sulphur butterflies.

No abstract

Preeclampsia (PE), new onset hypertension during pregnancy, affects 5‐7% of all pregnancies in the U.S. and is associated with reduced fetal weight, increased inflammation, vascular endothelial dysfunction (increased endothelin‐1 (ET‐1) and decreased nitric oxide (NO)) and hypertension. To date the best treatment remains early delivery of the feto‐placental unit. Activated lymphocytes during normal pregnancy (NP) express progesterone receptors, which stimulate a protein called Progesterone Induced Blocking Factor (PIBF) that is reduces during hypertensive pregnancy disorders. Therefore, this study was designed to test the hypothesis that progesterone, in the form of 17‐hydroxyprogesterone caproate (17‐OHPC), reduces inflammation, markers of endothelial dysfunction while reducing blood pressure and prolong time to delivery in PE women. In our ongoing clinical trial, PE participants received 17‐OHPC (250 mg, I.M.) with blood draws before and after injection. Placentas were collected at delivery. PIBF was 18.6 +/‐1.0 pg/mL in NT (n=4), 14.53 +/‐ 1.0 pg/mL in PE (n=10, p<0.05), and 15.78 +/‐0.85 in PE+17‐OHPC (n=6). Placental CD4+ T cells were 6.5+/‐ 2.7 in PE (n=3), 4.6+/‐ 2.0 in PE +17‐OHPC (n=4). Circulating CD4+ T cells were 18.23 +/‐4.8 in PE (n=4), 14.4+/‐1.2 % gate in PE+17‐OHPC (n=5). Placental TH2 cells were 81.7+/‐10.6% gate in PE and 84.7+/‐11.0 in PE+17‐OHPC. Placental and circulating NK cells were 20.84 +/‐ 6.8 % gate, 7.2 +/‐ 2.0 in PE which reduced to 4.7+/‐1.03, 5.3 +/‐ 1.5 % gate in PE+17‐OHPC. Circulating TNF‐alpha was 32.0 +/‐ 3.4 pg/mL in PE (n=8), which decreased to 21.1+/‐5.5 in PE+17OHPC (n=4). Circulating ET‐1 was 2.53+/‐ 0.4 pg/mL in healthy normal pregnant (NP, n=5), 6.7 +/‐ 1.4 in PE (n=18, p<0.05) and 4.9 +/‐ 1.3 in PE+17‐OHPC. Placenta preproendothelin ‐1 (PPET‐1) increased 1.5 fold change in PE (n=4) compared to NP, which was reduced to 0.96 in PE+17‐OHPC (n=4). Importantly, endotheling‐1 measured in HUVECS media treated with PE sera was 68 +/‐ 22 pg/mg of protein in PE which reduced to 57 +/‐19 in PE+17OHPC (n=6). Moreover, circulation nitrate‐nitrite was 50 +/‐ 9 uM in PE and significantly increased to 94 +/‐14 in PE+17‐OHPC. 17‐OHPC prolonged time of delivery beyond 72h on average and average systolic blood pressure was 151 +/‐ 5 mmHg in PE (n=18) and 137+/‐4 in PE+17‐OHPC (n=13). Our results suggest that 17‐OHPC reduced inflammation, markers of endothelial dysfunction, lowered blood pressure and prolonged time do delivery in PE women.