Our results establish that the bacterial H-NS nucleoprotein filament, a central organizer of the bacterial nucleoid structure, can slow transcript elongation by RNAP and increase Rho-dependent termination by increasing transcriptional pausing at specific sites.
We conclude that H-NS filaments can drastically slow transcript elongation by ECs under physiological conditions that would prevail when E. coli grows at ambient temperatures outside a mammalian host.
Microarray gene-expression analysis confirmed enhanced fast-fiber isoforms, repressed slow-fiber transcripts, and reduced neonatal fiber transcripts in the mitochondrial myopathy.
As demonstrated by in situ hybridization technique, in human type I fibers the corresponding 1 or β-slow MyHC transcripts were predominantly expressed, but they seemed to be expressed in some type II fibers as well.
VpCDPK6 (Additional file 3) and VpCDPK19 (Fig. 7-b) shared similar expression patterns, with a slow increase in transcript levels to a peak and gradual plateau.
In the first case, if the transition rates between active and inactive states are extremely slow relative to transcript and protein degradations, each promoter state would be relatively stable, and this transcription regime could result in bi-modal protein expression [ 4- 6].
About half of total transcripts can be detected in any one of the lanes sequenced for G4 or S4 (Figure S11), and increasing the number of lanes counted leads to slow increase of transcripts detected (Figure S12), indicating that sequencing in one lane is efficient to do expression profiling and deep sequencing data are the most informative.
The majority (34 out of 46) of the recovered transcripts are predicted to encode full-length proteins despite the fact that many plastochron-related genes, including ERECTA, ERECTA LIKE-1, SERRATE and SLOW MOTION, yield transcripts close to 3 kb or greater.
The cardiac TnI (cTnI) and the slow skeletal TnI (ssTnI) transcripts coexist in the developing heart throughout fetal and perinatal stages and then cTnI completely replaces ssTnI in the adolescent mouse [4], [5].
Rather, being a noncoding transcript has slowed the process of shading light on its mechanisms of action, for reasons of both technical and cultural nature.
Genes in cluster C displayed a sustained, slower increase of their transcript levels than those in clusters A and B. 37% of the genes in cluster C encoded ribosomal proteins.
