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Category: Microbial Genetics and Molecular Biology
Cross-Regulation between Bacteria and Phages at a Posttranscriptional Level, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781683670247/9781683670230_Chap29-1.gif /docserver/preview/fulltext/10.1128/9781683670247/9781683670230_Chap29-2.gifAbstract:
The impact that the study of phages, both in their lytic form and as prophages integrated into bacterial chromosomes, has had on molecular biology and microbiology is hard to overstate. The ease of phage manipulation helped establish several of the central dogmas in molecular biology. For example, characterization of various phage DNA polymerases contributed to the understanding of replication ( 1 , 2 ), and models of transcription regulation were greatly influenced by studies of cI, the phage λ repressor ( 3 , 4 ). Phages also have continually provided important tools such as transduction, the phage-assisted movement of DNA from one bacterium to another, which has been an essential tool since the early years of molecular biology ( 5 , 6 ). As another example, the development of chain termination DNA-sequencing approaches benefited from single-stranded DNA cloning vectors derived from phage M13 ( 7 ).
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Repression of both prophage- and bacterial-encoded mRNAs by sRNAs encoded by horizontally acquired elements and the bacterial core genome. (A) Following host-cell invasion, the prophage-encoded sRNA PinT (purple) is activated by the core genome-encoded transcription factor PhoP (blue). PinT is an Hfq-binding sRNA that regulates multiple target genes through direct base-pairing. These include the mRNAs of the two horizontally acquired effector proteins, SopE and SopE2, as well as the core genome-encoded crp mRNA. The Crp protein acts as an activator of SPI-2 (intracellular) virulence genes of S. enterica. (B) The core genome-encoded (blue) OxyS sRNA is activated by the OxyR transcription factor under conditions of oxidative stress. OxyS associates with Hfq to regulate at least two targets: the mRNA encoding the FhlA transcription regulator of formate metabolism and the transcript encoding NusG, an important transcription termination factor. OxyS repression of NusG, which normally blocks expression of the prophage-encoded (purple) KilR protein together with the Rho termination factor, results in increased production of KilR, which transiently inhibits cell division.
Prophage-encoded sRNAs that regulate the expression of host genes. (A) The prophage-encoded (purple) sRNA DicF is processed from a polycistronic transcript by RNase E, and, for the second DicF isoform, by RNase III. DicF associates with Hfq to repress synthesis of the core genome-encoded (blue) FtsZ protein, required for cell division, as well as XylR, PykA, and ManX, all involved in carbon metabolism. (B) Esr41 is a prophage-encoded (purple) sRNA that binds Hfq to inhibit translation of the core genome-encoded (blue) cirA, chuA, and bfr mRNAs. The gene products of the mRNAs are involved in iron metabolism, and repression of cirA results in colicin resistance. Esr41 also leads to increased motility by upregulation of FliC; however, the molecular mechanism underlying this process has not yet been determined.
Prophage-encoded and core genome-encoded sRNAs that act as sponges to block the activities of core-encoded sRNAs. The prophage-encoded (purple) AgvB sRNA, as well as the core genome-encoded sRNA (blue) SroC use Hfq to base-pair with the GcvB sRNA to inhibit the function of the GcvB global regulator of amino acid uptake and metabolism. SroC is generated from RNase E-mediated endonucleolytic processing of a polycistronic transcript, while AgvB is transcribed from a freestanding gene.
Examples of posttranscriptional cross-regulation between bacteria and phages