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. 2019 Jun 24;5:107. doi: 10.1038/s41420-019-0187-1

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Merozoite egress and host cell membrane permeabilization was monitored by time-lapse microscopy in the presence of 100 μM Phalloidin Alexa 488. Host cell membrane permeabilization accompanied by egress of merozoites was observed following propranolol (125 μM) treatment of parasites while untreated parasites did not demonstrate preterm egress. b Egress of merozoites was quantified using Giemsa staining and visualized under microscope. The counting data demonstrated that propranolol (125 μM) treatment induced approx. two-fold egress as compared to control. **P < 0.01, (n = 3). (c) Host cell membrane permeabilization in the presence of propranolol (125 μM). (i) Percent of phalloidin positive schizonts, demonstrating host erythrocyte membrane permeabilization, increased in the presence of propranolol. **P < 0.01, (n = 2) (ii) Corresponding confocal images of the treated and untreated schizonts in the presence of Phalloidin Alexa 488. d Localization of PLP1 on host erythrocyte membrane. (i) Propranolol (125 μM) treated and untreated schizonts were stained with anti-PLP1 antibody and visualized under confocal microscope. 3-D reconstruction of the confocal images by IMARIS is also shown. PLP1 is localized more on host erythrocyte membrane as compared to untreated control. (ii) To score the increased localization of PLP1 on membrane, we created ROI specific to membrane of RBC and analyzed intensity of PLP1 staining. The results demonstrate that propranolol treated schizonts have higher intensity of PLP1 on membrane as compared to control. e Microneme secretion is triggered in the presence of propranolol (125 μM). Merozoites were isolated and incubated in the presence and absence of BAPTA-AM and propranolol. Microneme secretion was assessed in the merozoite supernatant. Enhanced AMA1, a micronemal marker, secretion was observed in supernatant of propranolol while BAPTA-AM was used as a negative control. NAPL worked as loading and lysis control

Fig. 4 — a Merozoite egress and host cell membrane permeabilization was monitored by time-lapse microscopy in the presence of 100 μM Phalloidin Alexa 488. Host cell membrane permeabilization accompanied by egress of merozoites was observed following propranolol (125 μM) treatment of parasites while untreated parasites did not demonstrate preterm egress. b Egress of merozoites was quantified using Giemsa staining and visualized under microscope. The counting data demonstrated that propranolol (125 μM) treatment induced approx. two-fold egress as compared to control. **P < 0.01, (n = 3). (c) Host cell membrane permeabilization in the presence of propranolol (125 μM). (i) Percent of phalloidin positive schizonts, demonstrating host erythrocyte membrane permeabilization, increased in the presence of propranolol. **P < 0.01, (n = 2) (ii) Corresponding confocal images of the treated and untreated schizonts in the presence of Phalloidin Alexa 488. d Localization of PLP1 on host erythrocyte membrane. (i) Propranolol (125 μM) treated and untreated schizonts were stained with anti-PLP1 antibody and visualized under confocal microscope. 3-D reconstruction of the confocal images by IMARIS is also shown. PLP1 is localized more on host erythrocyte membrane as compared to untreated control. (ii) To score the increased localization of PLP1 on membrane, we created ROI specific to membrane of RBC and analyzed intensity of PLP1 staining. The results demonstrate that propranolol treated schizonts have higher intensity of PLP1 on membrane as compared to control. e Microneme secretion is triggered in the presence of propranolol (125 μM). Merozoites were isolated and incubated in the presence and absence of BAPTA-AM and propranolol. Microneme secretion was assessed in the merozoite supernatant. Enhanced AMA1, a micronemal marker, secretion was observed in supernatant of propranolol while BAPTA-AM was used as a negative control. NAPL worked as loading and lysis control