XRE transcription factors conserved in Caulobacter and φCbK modulate adhesin development and phage production.
XRE transcription factors conserved in Caulobacter and φCbK modulate adhesin development and phage production.
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DOI：
10.1371/journal.pgen.1011048
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发表时间：
2023-11
期刊：
影响因子：
4.5
通讯作者：
中科院分区：
文献类型：
--
作者：
异生素反应元件（XRE）家族的转录因子（TF）通常由细菌和噬菌体编码，调节细菌细胞生理学的不同特征并影响噬菌体感染动力学。通过对从土壤和水生生态系统中分离的柄杆菌属物种的泛基因组分析，我们发现了一个明显的旁系同源XRE TF基因簇的辐射，其中一些基因簇在调节柄杆菌中的固着粘附素发育和生物膜形成中具有确定的功能。crescentus。我们进一步发现了贯穿α变形菌纲及其分支的相关XRE TF，包括φCbK柄噬菌体，表明该簇的成员影响宿主-噬菌体相互作用。在这里，我们表明，一组密切相关的XRE转录因子编码的两个C。crescentus和φCbK可以物理地相互作用并起作用以控制共同基因集的转录，影响包括固着发育和φCbK病毒粒子的产生的过程。φ CbK编码的XRE蛋白tgrL在感染的最早阶段高度表达，并且可以直接抑制宿主基因的转录，包括hfiA（一种有效的固着抑制剂）和gafYZ（一种前噬菌体样基因转移剂（GTA）的激活剂）。从C. crescentus染色体也直接抑制gafYZ转录，揭示了一组功能冗余的宿主调节因子，其可以防止GTA颗粒的假产生和无意的细胞裂解。删除C。crescentus XRE转录因子减少了φCbK爆发大小，而过表达这些宿主基因或φCbK tgrL挽救了这种爆发缺陷。我们的结论是，该XRE TF基因簇，共享C。crescentus和φCbK在无噬菌体条件下的粘附调节中起重要作用，并影响感染期间宿主-噬菌体动力学。在感染期间，细菌和它们的病毒（即噬菌体）调节彼此的转录以促进它们自身的适应性。一组广泛保守的蛋白质通常参与宿主和病毒之间的这场战斗，是转录因子（TF）的异生素反应元件（XRE）家族。我们确定了一个保守的XRE TF基因簇中的Alphaproteobacteria和他们的噬菌体。在新月柄杆菌及其噬菌体φCbK中，这些密切相关的转录因子调节影响柄杆菌粘附和噬菌体病毒体产生的共同基因集。我们测量了φCbK基因组在整个感染周期中的转录，发现噬菌体XRE TF基因tgrL在感染的最早阶段高度表达，我们提出了TgrL增强φCbK适应性的证据。我们的研究结果提供了一个例子，如何进化相关的一组转录因子，发现在主机和它的病毒，影响主机的防御机制和病毒的健身。
The xenobiotic response element (XRE) family of transcription factors (TFs), which are commonly encoded by bacteria and bacteriophage, regulate diverse features of bacterial cell physiology and impact phage infection dynamics. Through a pangenome analysis of Caulobacter species isolated from soil and aquatic ecosystems, we uncovered an apparent radiation of a paralogous XRE TF gene cluster, several of which have established functions in the regulation of holdfast adhesin development and biofilm formation in C. crescentus. We further discovered related XRE TFs throughout the class Alphaproteobacteria and its phages, including the φCbK Caulophage, suggesting that members of this cluster impact host-phage interactions. Here we show that a closely related group of XRE transcription factors encoded by both C. crescentus and φCbK can physically interact and function to control the transcription of a common gene set, influencing processes including holdfast development and the production of φCbK virions. The φCbK-encoded XRE paralog, tgrL, is highly expressed at the earliest stages of infection and can directly inhibit transcription of host genes including hfiA, a potent holdfast inhibitor, and gafYZ, an activator of prophage-like gene transfer agents (GTAs). XRE proteins encoded from the C. crescentus chromosome also directly repress gafYZ transcription, revealing a functionally redundant set of host regulators that may protect against spurious production of GTA particles and inadvertent cell lysis. Deleting the C. crescentus XRE transcription factors reduced φCbK burst size, while overexpressing these host genes or φCbK tgrL rescued this burst defect. We conclude that this XRE TF gene cluster, shared by C. crescentus and φCbK, plays an important role in adhesion regulation under phage-free conditions, and influences host-phage dynamics during infection. During infection, bacteria and their viruses (i.e. phage) modulate each other’s transcription to promote their own fitness. A broadly conserved group of proteins that are commonly engaged in this battle between host and virus are the xenobiotic response element (XRE) family of transcription factors (TFs). We identified a conserved cluster of XRE TF genes in Alphaproteobacteria and their bacteriophage. In Caulobacter crescentus and its phage, φCbK, these closely related transcription factors regulate a common gene set that impacts Caulobacter adhesion and phage virion production. We measured transcription of the φCbK genome across an infection cycle and discovered that the phage XRE TF gene, tgrL, is highly expressed at the earliest stages of infection, and we present evidence that TgrL enhances φCbK fitness. Our results offer an example of how an evolutionarily related set of transcription factors, found in both a host and its virus, influence host defense mechanisms and viral fitness.
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影响因子：
14.9
作者：
Blum M;Chang HY;Chuguransky S;Grego T;Kandasaamy S;Mitchell A;Nuka G;Paysan-Lafosse T;Qureshi M;Raj S;Richardson L;Salazar GA;Williams L;Bork P;Bridge A;Gough J;Haft DH;Letunic I;Marchler-Bauer A;Mi H;Natale DA;Necci M;Orengo CA;Pandurangan AP;Rivoire C;Sigrist CJA;Sillitoe I;Thanki N;Thomas PD;Tosatto SCE;Wu CH;Bateman A;Finn RD
通讯作者：
Finn RD
影响因子：
3.6
作者：
Frederix M;Edwards A;Swiderska A;Stanger A;Karunakaran R;Williams A;Abbruscato P;Sanchez-Contreras M;Poole PS;Downie JA
通讯作者：
Downie JA
影响因子：
4.2
作者：
da Silva CA;Lourenço RF;Mazzon RR;Ribeiro RA;Marques MV
通讯作者：
Marques MV
DOI：
10.1093/plcell/koac076
发表时间：
2022-07-04
期刊：
The Plant cell
影响因子：
--
作者：
通讯作者：
--
影响因子：
7.7
作者：
Barth ZK;Nguyen MH;Seed KD
通讯作者：
Seed KD