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首页> 外文期刊>Current Biology: CB >Intertissue Mechanical Stress Affects Frizzled-Mediated Planar Cell Polarity in the Drosophila Notum Epidermis
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Intertissue Mechanical Stress Affects Frizzled-Mediated Planar Cell Polarity in the Drosophila Notum Epidermis

机译:组织间机械应力影响果蝇Notum表皮中的毛躁介导的平面细胞极性。

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Frizzled/planar cell polarity (Fz/PCP) signaling controls the orientation of sensory bristles and cellular hairs (trichomes) along the anteroposterior axis of the Drosophila thorax (notum) [[1], [2], [3] and [4]]. A subset of the trichome-producing notum cells differentiate as "tendon cells," serving as attachment sites for the indirect flight muscles (IFMs) to the exoskeleton [5]. Through the analysis of chascon (chas), a gene identified by its ability to disrupt Fz/PCP signaling under overexpression conditions, and jitterbug (jbug)/filamin [6], we show that maintenance of anteroposterior planar polarization requires the notum epithelia to balance mechanical stress generated by the attachment of the IFMs. chas is expressed in notum tendon cells, and its loss of function disturbs cellular orientation at and near the regions where IFMs attach to the epidermis. This effect is independent of the Fz/PCP and fat/dachsous systems [7]. The chas phenotype arises during normal shortening of the IFMs [8] and is suppressed by genetic ablation of the IFMs. chas acts through jbug/filamin and cooperates with MyosinII to modulate the mechanoresponse of notum tendon cells. These observations support the notion that the ability of epithelia to respond to mechanical stress generated by one or more interactions with other tissues during development and organogenesis influences the maintenance of its shape and PCP features. Highlights: chas is required to orient notum bristles and trichomes along the body axis chas-jbug/filamin act in parallel to Fz/PCP signaling to polarize the notum epidermis chas-jbug/filamin and MyoII modulate the mechanoresponse of notum tendon cells Mechanical adaptation upon intertissue interaction is required to preserve PCP
机译:毛躁/平面细胞极性(Fz / PCP)信号控制果蝇胸部(notum)前后轴的感觉毛和细胞毛(毛状体)的方向[[1],[2],[3]和[4] ]。产生毛状体的Notum细胞的一个子集分化为“肌腱细胞”,充当间接飞行肌肉(IFM)与外骨骼的附着位点[5]。通过对chascon(chas)的分析,该基因由其在过表达条件下破坏Fz / PCP信号的能力和jitterbug(jbug)/ filamin [6]鉴定的能力,我们表明维持前后平面极化需要平衡上皮平衡由IFM附着产生的机械应力。 chas在Notum肌腱细胞中表达,其功能丧失会干扰IFM附着于表皮的区域及其附近的细胞方向。这种作用与Fz / PCP和脂肪/脂肪系统无关[7]。 Chas表型在IFM的正常缩短过程中出现[8],并被IFM的遗传切除所抑制。 chas通过jbug / filamin起作用,并与MyosinII协同调节Notum肌腱细胞的机械反应。这些观察结果支持这样的观点,即上皮对发育和器官发生过程中与其他组织的一种或多种相互作用产生的机械应力作出反应的能力会影响其形状和PCP功能的维持。亮点:需要chas才能沿着身体轴定向notum刚毛和毛状体chas-jbug / filamin与Fz / PCP信号平行地作用,以极化notum表皮chas-jbug / filamin和MyoII调节notum肌腱细胞的机械反应组织间相互作用是保护PCP所必需的

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