Evidence that putrescine acts as an extracellular signal required for swarming in Proteus mirabilis
Evidence that putrescine acts as an extracellular signal required for swarming in Proteus mirabilis
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DOI：
10.1046/j.1365-2958.2003.03835.x
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发表时间：
2004-01-01
影响因子：
3.6
通讯作者：
Rather, PN
中科院分区：
文献类型：
--
作者：
Sturgill, G;Rather, PN
在寻找受细胞间信号调节的奇异变形杆菌基因的过程中，发现了一种lacZ融合基因（cmr437::mini-Tn5lacZ）被野生型细胞自我产生的细胞外信号抑制了10倍。然而，cmr437::mini-Tn5lacZ插入本身导致这种细胞外抑制信号的显著减少。cmr437::mini-Tn5lacZ插入在P. mirabilis中被定位到一个speA同源物。序列分析表明speA下游编码speB同源物。测定了SpeA和SpeB酶产物（agmatine和腐胺）对cmr437::lacZ的抑制作用。胍丁氨酸不具有抑制活性。然而，腐胺是一种有效的抑制分子，浓度低至30mum。cmr437 (speA)::mini-Tn5lacZ插入的第二个突出表型是群体运动的严重缺陷。在含有下游speB基因断裂的菌株中也观察到这种群体缺陷。与野生型细胞相比，speB突变体向群集细胞的分化延迟了2小时。此外，speB突变体不能有效地在琼脂表面迁移，形成非常紧密间隔的群体环。外源性腐胺恢复了蜂拥细胞分化的正常时间和向speB突变体迁移的能力。
In a search for Proteus mirabilis genes that were regulated by cell-to-cell signalling, a lacZ fusion (cmr437::mini-Tn5lacZ) was identified that was repressed 10-fold by a self-produced extracellular signal from wild-type cells. However, the cmr437::mini-Tn5lacZ insertion itself led to a marked reduction in this extracellular repressing signal. The cmr437::mini-Tn5lacZ insertion was mapped to a speA homologue in P. mirabilis. Sequence analysis indicated that a speB homologue was encoded downstream of speA. Products of the SpeA and SpeB enzymes (agmatine and putrescine) were tested for repression of cmr437::lacZ. Agmatine did not have repressing activity. However, putrescine was an effective repressing molecule at concentrations down to 30 muM. A second prominent phenotype of the cmr437 (speA)::mini-Tn5lacZ insertion was a severe defect in swarming motility. This swarming defect was also observed in a strain containing a disruption of the downstream speB gene. Differentiation of the speB mutant to swarmer cells was delayed by two hours relative to wild-type cells. Furthermore, the speB mutant was unable to migrate effectively across agar surfaces and formed very closely spaced swarming rings. Exogenous putrescine restored both the normal timing of swarmer cell differentiation and the ability to migrate to speB mutants.