Plasmid ColE1 incompatibility determined by interaction of RNA I with primer transcript.

Tomizawa, Jun-ichi; Itoh, Tateo

doi:10.1073/pnas.78.10.6096

Cited by 232 publications

(117 citation statements)

References 24 publications

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“…The first and second loops (I' and II') of RNAIPKY _1 have the same sequences as those of C1oDF 13, but the third one has that of ColE 1. It was suggested that the incompatibility of the ColE 1-type plasmids occurred as a result of the interaction of the nucleotides in these loops with the primer RNA (3,4). The difference between loops I' and II' of pKY-1 RNAI and those of Co1E1 supports the fact that the former is compatible with the latter.…”

Section: Discussionsupporting

confidence: 73%

The nucleotide sequence of cea* and the region of origin of plasmid pKY-1.

Higashi¹,

Hata²,

Hase³

et al. 1986

J. Gen. Appl. Microbiol.

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Section: Discussionsupporting

confidence: 73%

The nucleotide sequence of cea* and the region of origin of plasmid pKY-1.

Higashi¹,

Hata²,

Hase³

et al. 1986

J. Gen. Appl. Microbiol.

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“…For DNA templates, we used pSR/ CC(Ϫ41.5) (26) and pSR/CC(Ϫ61.5) (27), which contain the OOP Rho factor-independent transcription terminator and which both produce a transcript of 123 nucleotides. The 108-nucleotide RNA I transcript served as a control (31). The pSR/CC(Ϫ41.5) and pSR/CC(Ϫ61.5) plasmids were prepared using a Qiagen miniprep kit and further purified by phenol extraction.…”

Section: Cloning Of Crp and Generation Of Mutants-e Coli Crp Was Clomentioning

confidence: 99%

Study of Highly Constitutively Active Mutants Suggests How cAMP Activates cAMP Receptor Protein

Youn

Kerby

Conrad

et al. 2006

Journal of Biological Chemistry

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“…For example, replication of the ColE1 plasmids is regulated by an antisense RNA, which by binding to a preprimer RNA alters its folding and prevents its subsequent processing to form a primer for the initiation of DNA synthesis (19,24,49,50). The antisense RNAs of the pT181, FII, IncI 1 and IncB plasmids inhibit the expression of the genes coding for the essential replication initiation proteins (Rep) (13,30,31,35,42,46).…”

mentioning

confidence: 99%

The replication of an IncL/M plasmid is subject to antisense control

1995

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A 2,385-bp sequence that contains the information for the autonomous replication of the IncL/M plasmid pMU604 was characterized. Genetic analyses revealed that the replicon specifies at least four structural genes, designated repA, repB, repC, and rnaI. The repA gene encodes a protein with a molecular weight of 40,861 which probably functions as an initiator for replication. The functions of the proteins of the repB and repC genes are unclear; however, mutations in the start codon of repB reduced the expression of both repB and repA, indicating that these two genes are translationally coupled. The rnaI gene encodes a small antisense RNA of about 75 to 77 bases and is responsible for the incompatibility phenotype, thus implicating its role as the main copy number determinant. RNAI exerts its effect in trans to repress the expression of repA at the posttranscriptional level. Furthermore, two complementary sequences of 8 bases, with the potential to interact and form a putative pseudoknot structure, were identified in the leader region of the repA mRNA. Base-pairing between the two complementary sequences was shown to be critical for efficient repA expression. A model for the regulation of pMU604 replication involving both translational coupling and pseudoknot formation is proposed.Plasmids that employ a system of copy number control that involves inhibitor molecules binding to target sequences generally regulate their replication via a small antisense RNA molecule. The target of this inhibitory RNA is the complementary region of a large RNA transcript, whose product is essential for replication. Both antisense and target RNAs are highly structured molecules capable of assuming stable stem-andloop configurations. These structural motifs are just as important as their primary sequences for efficient and specific interaction between antisense and target molecules (6,10,32,34,43,47,52). Because the small RNAs act in trans, they are also able to affect the replication of other plasmids showing the same specificity of replication control. The ability to interact with the replication machinery of other plasmids means that antisense RNAs act as incompatibility determinants (29).Although a number of plasmids use antisense RNA to regulate the frequency with which they initiate replication, the particular molecular mechanism differs for each system. For example, replication of the ColE1 plasmids is regulated by an antisense RNA, which by binding to a preprimer RNA alters its folding and prevents its subsequent processing to form a primer for the initiation of DNA synthesis (19,24,49,50). The antisense RNAs of the pT181, FII, IncI 1 and IncB plasmids inhibit the expression of the genes coding for the essential replication initiation proteins (Rep) (13,30,31,35,42,46). In pT181, binding of the antisense alters the folding of the rep mRNA, resulting in transcriptional attenuation of the message (31). Control of copy number in the FII plasmids R1 and NR1 involves the hybridization of the antisense RNA with its complementary sequ...

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Plasmid ColE1 incompatibility determined by interaction of RNA I with primer transcript.

Cited by 232 publications

References 24 publications

The nucleotide sequence of cea* and the region of origin of plasmid pKY-1.

The nucleotide sequence of cea* and the region of origin of plasmid pKY-1.

Study of Highly Constitutively Active Mutants Suggests How cAMP Activates cAMP Receptor Protein

The replication of an IncL/M plasmid is subject to antisense control

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