Nishimura Mayuko, Nagashio Ryo, Sato Yuichi, Hasegawa Takayuki
Section of Biology, College of Liberal Arts and Sciences, Kitasato University, Sagamihara, Kanagawa, 252-0373, Japan.
Department of Applied Tumor Pathology, Graduate School of Medical Sciences, Kitasato University, Kanagawa, 252-0373, Japan.
Planta. 2017 Jan;245(1):183-192. doi: 10.1007/s00425-016-2599-y. Epub 2016 Oct 3.
We identified LSG2 as a novel lytic enzyme that accumulates in the parental extracellular matrix and disrupts parental spheroids cooperatively with VheA secreted by juveniles in Volvox. Spatiotemporally restricted degradation of extracellular matrix (ECM) is essential for development and survival in multicellular organisms. In an asexual life cycle of green algae Volvox, juveniles are released from parental spheroids through holes made by restricted degradation of parental ECM at the proper timing. Lytic enzyme(s) should specifically degrade parental ECM upon Volvox hatching, but little is known about the mechanisms of spatiotemporally restricted parental degradation. Here, we identified a glycoprotein encoded by the Late Somatic Gene 2 (LSG2) as a novel lytic enzyme that accumulates in parental ECM during the prehatching stages. The dual action of LSG2 and Volvox hatching enzyme A (VheA), a serine protease secreted by juveniles, causes the degradation of ECM sheets at all stages and destroys even daughter spheroids, while VheA alone disrupts spheroids only in the prehatching stage when LSG2 is accumulated, suggesting that the combination of LSG2 and VheA is sufficient to cause the degradation of ECM sheet. In the prehatching stage, parental spheroids became susceptible to the proteolysis by a mixture of bacterial proteases applied externally, which could be facilitated by LSG2. These results suggest that LSG2 disrupts parental ECM cooperatively with VheA by modifying the parental ECM to make it fragile, and that the appropriate activity of these enzymes is crucial for the parent-specific ECM degradation at the proper timing.
我们鉴定出LSG2是一种新型裂解酶,它积聚在亲代细胞外基质中,并与团藻幼体分泌的VheA协同破坏亲代球体。细胞外基质(ECM)的时空受限降解对于多细胞生物的发育和生存至关重要。在绿藻团藻的无性生命周期中,幼体通过在适当时间对亲代ECM进行受限降解形成的孔从亲代球体中释放出来。裂解酶应在团藻孵化时特异性降解亲代ECM,但关于时空受限的亲代降解机制知之甚少。在这里,我们鉴定出一种由晚期体细胞基因2(LSG2)编码的糖蛋白作为一种新型裂解酶,它在孵化前阶段积聚在亲代ECM中。LSG2和团藻孵化酶A(VheA,一种由幼体分泌的丝氨酸蛋白酶)的双重作用导致ECM片层在所有阶段降解,甚至破坏子球体,而单独的VheA仅在LSG2积累的孵化前阶段破坏球体,这表明LSG2和VheA的组合足以导致ECM片层的降解。在孵化前阶段,亲代球体对外源施加的细菌蛋白酶混合物变得易受蛋白水解作用,而LSG2可以促进这种作用。这些结果表明,LSG2通过修饰亲代ECM使其变得脆弱,从而与VheA协同破坏亲代ECM,并且这些酶的适当活性对于在适当时间进行亲代特异性ECM降解至关重要。