# The _E. coli_ Global Regulator DksA Reduces Transcription during T4 Infection
## 3 Results
### Deletion of dksA Results in a Shorter Latent Period in a T4 motA\({}^{am}\) Infection
As seen in Figure 3, within regions that contain both Pe's and Pm's, we observed two sections of T4 genes that are crucial for replication and late transcription and are highly dependent on MotA: (1) the region downstream of Pe35.3 (map units 35,662 to 27,197) that includes gene 43 (DNA polymerase), gene 45 (DNA polymerase clamp and late transcription enhancer), and genes 44/62 (clamp loader) and (2) the region downstream of Pe148.6 (map units 150,727 to 146,948) that includes gene 33 (co-activator required for late transcription), \(rnh\) (RNase H), gene 59 (DNA helicase loader for replication), and gene 32 (single-stranded DNA binding protein). However, other sections with Pe's and Pm's, whose genes also encode important replication and late transcription factors, were not significantly MotA-dependent. These included: (1) the region downstream of Pe26.4, Pe20.3, and Pe19.8  
Figure 4: RNA from Pe148.6, which is significantly reduced in a T4\(motA^{am}\) infection of B606 wt at 5 min post-infection, is rescued by a deletion of DksA. (**a**) Schematic showing T4 map units from 150,727 to 149,509 containing genes \(rnh\) and \(dsbA\) with the relative positions of the early promoter Pe148.6 and the middle promoter Pm\(dsbA\) and the primers used for primer extension analyses. Sizes of the expected primer extension products are indicated in nts; (**b**) Representative gel showing the primer extension products from primers indicated in panel (a). RNA was isolated from T4 wt (+) or T4\(motA^{am}\) (\(am\)) infections of strain B606 wt (+) or B606 \(\Delta dsA\) (–) at 5 or 1 min post-infection. (map units 27,044 to 17,935) containing genes 41/61 (DNA helicase/primase) and _uvsX_ (_recA_ analog), and (2) the region downstream of Pe40.4 (map units 41,225 to 39,600) containing gene 55 (sigma factor for late transcription). Because the Pm's for both these regions (Pm55 and PmuvsX) are highly dependent on MotA (Figure S6a), we conclude that it is the extension of Pe's into these regions that compensates for the lack of MotA. Thus, our analyses indicate that at 5 min post-infection in the _motA_ knockdown, the expression of only a subset of middle genes encoding replication/recombination proteins was near wt levels. These include the genes for helicase (gp41), the recombination protein UvsX, EndoVII (gp49) that resolves recombination structures, nucleases gp46 and gp47, and DNA ligase (gp30). Such a combination of proteins suggests a minimal system for recombination in which nucleases 46/47 might generate ssDNA substrates suitable for homologous recombination by UvsX/gp41. The nicked DNA would then be sealed by DNA ligase. However, whether such a system is used is not known. Unexpectedly, RNA-seq indicated that the expression of two late genes, \(t\) (holm, map units 160,221 to 160,877) and 38 (catalyzes assembly of distal tail fibers, map units 159,649 to 160,200), increased in the T4_motA_m_ infection (Figure 3). We confirmed increased levels for both by RT-qPCR (Figure S5a). Given the significantly reduced levels of expression of T4 genes 45 and 33, whose products are required for late transcription, this result suggests an unusual expression mechanism for these late genes.