A regulatory cascade controls Staphylococcus aureus pathogenicity island activation.
A regulatory cascade controls Staphylococcus aureus pathogenicity island activation.
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DOI：
10.1038/s41564-021-00956-2
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发表时间：
2021-10
影响因子：
28.3
通讯作者：
Penadés JR
中科院分区：
文献类型：
--
作者：
Haag AF;Podkowik M;Ibarra-Chávez R;Gallego Del Sol F;Ram G;Chen J;Marina A;Novick RP;Penadés JR
葡萄球菌致病性岛（Staphylococcal pathogenicity islands，SaPI）是一个紧密相关的移动的染色体岛家族，编码和传播超抗原毒素TSST-1和SEB。它们由主阻遏物调节，主阻遏物被辅助噬菌体编码的蛋白质抵消，从而诱导它们的切除、复制、包装和细胞间转移。SaPI是葡萄球菌活动组的主要成分，占据5个染色体att位点，许多菌株含有2个或更多个。由于共同居住的SaPI之间的调节相互作用可能对超抗原病理生物学的传播产生深远的影响，我们开始了目前的研究，以寻找这种相互作用。使用经典遗传学，我们发现，除了一个例外，它们的调控系统不会交叉反应。唯一的例外是SaPI 3，它最初被认为是有缺陷的，因为它不能被任何已知的辅助噬菌体动员。我们在这里表明，SaPI 3具有非典型的调节模块，并且不是由噬菌体而是由许多其他SaPIs诱导，包括SaPI 2，SaPIbov 1和SaPIn 1，每个编码保守蛋白Sis，其抵消SaPI 3阻遏物，产生细胞内调节级联：当通常由辅助噬菌体诱导时，共存的SaPI表达其sis基因，该sis基因又诱导SaPI 3，使其能够扩散。利用生物信息学分析，我们已经鉴定了超过30个密切相关的共同祖先SEB编码的SaPI 3亲属，占据相同的att位点，并由保守的调控模块immA-immR-str '控制。该模块在功能上类似于但与典型的SaPI调节模块stl-str无关。由于SaPI是噬菌体卫星，SaPI 3及其亲属是SaPI卫星。
Staphylococcal pathogenicity islands (SaPIs) are a family of closely related mobile chromosomal islands that encode and disseminate the superantigen toxins, TSST-1 and SEB. They are regulated by master repressors, which are counteracted by helper phage-encoded proteins, thereby inducing their excision, replication, packaging and intercell transfer. SaPIs are major components of the staphylococcal mobilome, occupying 5 chromosomal att sites, many strains harbouring 2 or more. As regulatory interactions between co-resident SaPIs could have profound effects on the spread of superantigen pathobiology, we initiated the current study to search for such interactions. Using classical genetics, we found that with one exception, their regulatory systems do not cross-react. The exception was SaPI3, which was originally considered defective because it could not be mobilized by any known helper phage. We show here that SaPI3 has an atypical regulatory module and is induced not by a phage but by many other SaPIs, including SaPI2, SaPIbov1 and SaPIn1, each encoding a conserved protein, Sis, which counteracts the SaPI3 repressor, generating an intracellular regulatory cascade: the co-resident SaPI, when conventionally induced by a helper phage, expresses its sis gene which, in turn, induces SaPI3, enabling it to spread. Using bioinformatics analysis, we have identified more than 30 closely related co-ancestral SEB-encoding SaPI3 relatives, occupying the same att site and controlled by a conserved regulatory module, immA-immR-str’. This module is functionally analogous to but unrelated to the typical SaPI regulatory module, stl-str. As SaPIs are phage satellites, SaPI3 and its relatives are SaPI satellites.
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影响因子：
3.7
作者：
Novick, Richard P.
通讯作者：
Novick, Richard P.
影响因子：
7.7
作者：
Bowring, Janine;Neamah, Maan M.;Penades, Jose R.
通讯作者：
Penades, Jose R.
影响因子：
16
作者：
Fillol-Salom, Alfred;Bacarizo, Julio;Penades, Jose R.
通讯作者：
Penades, Jose R.
DOI：
10.1073/pnas.1406749111
发表时间：
2014-10-07
影响因子：
11.1
作者：
Ram, Geeta;Chen, John;Novick, Richard P.
通讯作者：
Novick, Richard P.
影响因子：
3.6
作者：
Ubeda, Carles;Maiques, Elisa;Penades, Jose R.
通讯作者：
Penades, Jose R.