A conserved signalling pathway for amoebozoan encystation that was co-opted for multicellular development.
A conserved signalling pathway for amoebozoan encystation that was co-opted for multicellular development.
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DOI：
10.1038/srep09644
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发表时间：
2015-04-16
影响因子：
4.6
通讯作者：
Schaap P
中科院分区：
文献类型：
--
作者：
Kawabe Y;Schilde C;Du Q;Schaap P
多细胞的进化需要新的细胞间通讯机制，但其起源尚不清楚。盘基骨柱细胞交换信号来定位多细胞孢子承载结构中的特化细胞类型。这些信号激活了复杂的通路，汇聚到camp依赖性蛋白激酶（PKA）的激活上。在Dictyostelid单细胞祖先中检测到控制PKA的基因，与大多数原生生物一样，它们在经历环境胁迫时会形成休眠囊肿。我们删除了中间种Polysphondylium中PKA和合成cAMP以激活PKA的腺苷酸环化酶AcrA和AcgA。Polysphondylium既可以发育成囊，也可以发育成多细胞结构。PKA的缺失阻止了多细胞发育，但也完全阻断了胞塞。AcrA和AcgA的缺失都是盘基骨菌产孢所必需的，但对多孢子菌的产孢没有影响，但阻止了胞积。我们的结论是，多细胞cAMP信号是通过PKA调控原生生物胞吞，并逐渐实现通路组分的再功能化而被吸收的。
The evolution of multicellularity required novel mechanisms for intercellular communication, but their origin is unclear. Dictyostelium cells exchange signals to position specialized cell types in multicellular spore-bearing structures. These signals activate complex pathways that converge on activation of cAMP-dependent protein kinase (PKA). Genes controlling PKA were detected in the Dictyostelid unicellular ancestors, which like most protists form dormant cysts when experiencing environmental stress. We deleted PKA and the adenylate cyclases AcrA and AcgA, which synthesize cAMP for PKA activation, in the intermediate species Polysphondylium, which can develop into either cysts or into multicellular structures. Loss of PKA prevented multicellular development, but also completely blocked encystation. Loss of AcrA and AcgA, both essential for sporulation in Dictyostelium, did not affect Polysphondylium sporulation, but prevented encystation. We conclude that multicellular cAMP signalling was co-opted from PKA regulation of protist encystation with progressive refunctionalization of pathway components.
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影响因子：
12.3
作者：
Sucgang R;Kuo A;Tian X;Salerno W;Parikh A;Feasley CL;Dalin E;Tu H;Huang E;Barry K;Lindquist E;Shapiro H;Bruce D;Schmutz J;Salamov A;Fey P;Gaudet P;Anjard C;Babu MM;Basu S;Bushmanova Y;van der Wel H;Katoh-Kurasawa M;Dinh C;Coutinho PM;Saito T;Elias M;Schaap P;Kay RR;Henrissat B;Eichinger L;Rivero F;Putnam NH;West CM;Loomis WF;Chisholm RL;Shaulsky G;Strassmann JE;Queller DC;Kuspa A;Grigoriev IV
通讯作者：
Grigoriev IV
DOI：
10.1126/science.1130670
发表时间：
2006-10-27
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Schaap P;Winckler T;Nelson M;Alvarez-Curto E;Elgie B;Hagiwara H;Cavender J;Milano-Curto A;Rozen DE;Dingermann T;Mutzel R;Baldauf SL
通讯作者：
Baldauf SL
影响因子：
14.9
作者：
Faix, J;Kreppel, L;Kimmel, AR
通讯作者：
Kimmel, AR
影响因子：
11.4
作者：
Thomason, PA;Traynor, D;Kay, RR
通讯作者：
Kay, RR
影响因子：
11.4
作者：
HOPPER, NA;HARWOOD, AJ;WILLIAMS, JG
通讯作者：
WILLIAMS, JG