Figure 5.
SRC-dependent polar cell internalization requires integrins but not Draper. (A) Quantifications of polar cell internalization from egg chambers at stage 10 for the indicated genotypes (see Materials and methods). Error bars: mean ± SEM (n = 3). The total number of clusters analyzed (n) is indicated at the top of each bar. Statistical significance was assessed with a Fisher exact test (one-tailed) and P values are shown at the top of the graph. ns indicates not significant. (B–D’’’) Single section from confocal images of border cell clusters from egg chambers at stage 9 expressing UAS-PLCδPHGFP (green) and the genotypes indicated. Egg chambers were stained with βPS (gray) and DAPI (blue). White or yellow asterisks indicate non-internalized or partially internalized polar cells, respectively. White arrows in D’’ point to the accumulation of βPS at the contact site(s) between border cell–polar cell. Images in B’’’–D’’’ indicate βPS staining in a Royal LUT, where white represents the highest amount of the protein and black the lowest one. Scale bar: 5 µm. Polar cells are outlined with a yellow dashed line in B’–D’. (E) Model of normal or elevated SRC activity in border cells. Top panels: In control border cell clusters, Rac activity is high in the lead cell protrusion and at the front of follower cells. Rho activity is localized posteriorly. When SRC is hyperactivated, it leads to the enrichment of Rac and Rho at the site of engulfment. Bottom panels: For clarity, only one border cell of the cluster is represented. Left: Wild-type border cells have normal levels of SRC activity. In this condition, cells are ovoid and no cannibalism of polar cells is observed. Most SRC is negatively regulated by CSK, but an active pool of the protein can phosphorylate Draper receptor or other targets, ensuring normal behavior. Integrin receptors remain inactive. Middle: SRC overexpression in border cells leads to a semicircular shape and limited polar cell cannibalism. Elevated SRC activity is sufficient to slightly increase pSHARK, but it is not enough to activate and recruit pFAK at border cell–polar cell contacts. Right: Hyperactivation of SRC causes border cells’ rounding and localized accumulation of active SRC at border cell–polar cell contacts. Localized SRC activity promotes the relocalization of Integrin receptors at the site of engulfment. FAK and SHARK tyrosine kinases are also activated and recruited by SRC to those contact sites. All these activated proteins serve as a node of signal amplification, triggering cannibalism of polar cells through the activation of Rac and Rho GTPases, F-actin, and Myosin. Dashed arrows represent a direct or indirect interaction.

SRC-dependent polar cell internalization requires integrins but not Draper. (A) Quantifications of polar cell internalization from egg chambers at stage 10 for the indicated genotypes (see Materials and methods). Error bars: mean ± SEM (n = 3). The total number of clusters analyzed (n) is indicated at the top of each bar. Statistical significance was assessed with a Fisher exact test (one-tailed) and P values are shown at the top of the graph. ns indicates not significant. (B–D’’’) Single section from confocal images of border cell clusters from egg chambers at stage 9 expressing UAS-PLCδPHGFP (green) and the genotypes indicated. Egg chambers were stained with βPS (gray) and DAPI (blue). White or yellow asterisks indicate non-internalized or partially internalized polar cells, respectively. White arrows in D’’ point to the accumulation of βPS at the contact site(s) between border cell–polar cell. Images in B’’’–D’’’ indicate βPS staining in a Royal LUT, where white represents the highest amount of the protein and black the lowest one. Scale bar: 5 µm. Polar cells are outlined with a yellow dashed line in B’–D’. (E) Model of normal or elevated SRC activity in border cells. Top panels: In control border cell clusters, Rac activity is high in the lead cell protrusion and at the front of follower cells. Rho activity is localized posteriorly. When SRC is hyperactivated, it leads to the enrichment of Rac and Rho at the site of engulfment. Bottom panels: For clarity, only one border cell of the cluster is represented. Left: Wild-type border cells have normal levels of SRC activity. In this condition, cells are ovoid and no cannibalism of polar cells is observed. Most SRC is negatively regulated by CSK, but an active pool of the protein can phosphorylate Draper receptor or other targets, ensuring normal behavior. Integrin receptors remain inactive. Middle: SRC overexpression in border cells leads to a semicircular shape and limited polar cell cannibalism. Elevated SRC activity is sufficient to slightly increase pSHARK, but it is not enough to activate and recruit pFAK at border cell–polar cell contacts. Right: Hyperactivation of SRC causes border cells’ rounding and localized accumulation of active SRC at border cell–polar cell contacts. Localized SRC activity promotes the relocalization of Integrin receptors at the site of engulfment. FAK and SHARK tyrosine kinases are also activated and recruited by SRC to those contact sites. All these activated proteins serve as a node of signal amplification, triggering cannibalism of polar cells through the activation of Rac and Rho GTPases, F-actin, and Myosin. Dashed arrows represent a direct or indirect interaction.

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