What Class Of Transposon Is Phage Mu
We report a new cellular interaction between the infecting transposable phage Mu and the host Escherichia coli replication machinery during repair of Mu insertions, which involves filling-in of short target gaps on either side of the insertion, concomitant with degradation of extraneous long flanking DNA (FD) linked to Mu. Using the FD as a marker to follow repair, we find that after transposition into the chromosome, the unrepaired Mu is indefinitely stable until the replication fork arrives at the insertion site, whereupon the FD is rapidly degraded. When the fork runs into a Mu target gap, a double strand end (DSE) will result; we demonstrate fork-dependent DSEs proximal to Mu. These findings suggest that Pol III stalled at the transpososome is exploited for co-ordinated repair of both target gaps flanking Mu without replicating the intervening 37kb of Mu, disassembling the stable transpososome in the process. This work is relevant to all transposable elements, including retroviral elements like HIV-1, which share with Mu the common problem of repair of their flanking target gaps.
Jun 30, 2015 - Transposable phage Mu has played a historic role in the. Has been used successfully for Mu integration in a variety of bacterial species,. The phage possesses the ability to integrate its genome into the bacterial chromosome without any site-specificity. Such random insertion of the phage genome into the bacterial chromosome causes mutation and, hence, the name of the phage (Mu stands for mutator). The phage Mu is, therefore, considered as a transposable agent.
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What Class Of Transposon Is Phage Mu Code
Abstract = 'We report a new cellular interaction between the infecting transposable phage Mu and the host Escherichia coli replication machinery during repair of Mu insertions, which involves filling-in of short target gaps on either side of the insertion, concomitant with degradation of extraneous long flanking DNA (FD) linked to Mu. Using the FD as a marker to follow repair, we find that after transposition into the chromosome, the unrepaired Mu is indefinitely stable until the replication fork arrives at the insertion site, whereupon the FD is rapidly degraded. When the fork runs into a Mu target gap, a double strand end (DSE) will result; we demonstrate fork-dependent DSEs proximal to Mu. These findings suggest that Pol III stalled at the transpososome is exploited for co-ordinated repair of both target gaps flanking Mu without replicating the intervening 37kb of Mu, disassembling the stable transpososome in the process.
This work is relevant to all transposable elements, including retroviral elements like HIV-1, which share with Mu the common problem of repair of their flanking target gaps.' TY - JOURT1 - Repair of transposable phage Mu DNA insertions begins only when the E.coli replisome collides with the transpososomeAU - Jang, SooinAU - Harshey, Rasika MPY - 2015/8/1Y1 - 2015/8/1N2 - We report a new cellular interaction between the infecting transposable phage Mu and the host Escherichia coli replication machinery during repair of Mu insertions, which involves filling-in of short target gaps on either side of the insertion, concomitant with degradation of extraneous long flanking DNA (FD) linked to Mu. Using the FD as a marker to follow repair, we find that after transposition into the chromosome, the unrepaired Mu is indefinitely stable until the replication fork arrives at the insertion site, whereupon the FD is rapidly degraded. When the fork runs into a Mu target gap, a double strand end (DSE) will result; we demonstrate fork-dependent DSEs proximal to Mu.
These findings suggest that Pol III stalled at the transpososome is exploited for co-ordinated repair of both target gaps flanking Mu without replicating the intervening 37kb of Mu, disassembling the stable transpososome in the process. This work is relevant to all transposable elements, including retroviral elements like HIV-1, which share with Mu the common problem of repair of their flanking target gaps.AB - We report a new cellular interaction between the infecting transposable phage Mu and the host Escherichia coli replication machinery during repair of Mu insertions, which involves filling-in of short target gaps on either side of the insertion, concomitant with degradation of extraneous long flanking DNA (FD) linked to Mu. Using the FD as a marker to follow repair, we find that after transposition into the chromosome, the unrepaired Mu is indefinitely stable until the replication fork arrives at the insertion site, whereupon the FD is rapidly degraded. When the fork runs into a Mu target gap, a double strand end (DSE) will result; we demonstrate fork-dependent DSEs proximal to Mu.
These findings suggest that Pol III stalled at the transpososome is exploited for co-ordinated repair of both target gaps flanking Mu without replicating the intervening 37kb of Mu, disassembling the stable transpososome in the process. This work is relevant to all transposable elements, including retroviral elements like HIV-1, which share with Mu the common problem of repair of their flanking target gaps.UR -10.1111/mmi.13061DO - 10.1111/mmi.13061M3 - ArticleVL - 97SP - 746EP - 758JO - Molecular MicrobiologyJF - Molecular MicrobiologySN - 0950-382XIS - 4ER.