Elongation arrest vs termination of transcription

Content
Expression of Gene : Protein Synthesis 2.  Transcription in Prokaryotes and Eukaryotes
Transcription in prokaryotes 
Single RNA polymerase in E. coli
Promoter sites for initiation of transcription in prokaryotes
Initiation and elongation of RNA synthesis in prokaryotes
'Inchworm model' for elongation of transcript
Elongation arrest vs termination of transcription
Termination and antitermination of mRNA synthesis in prokaryotes
Transcription in eukaryotes 
Multiple RNA polymerases in eukaryotes
Promoter, enhancer and silencer sites for initiation of transcription in eukaryotes
Transcription factors and initiation of RNA synthesis in eukaryotes
Formation of preinitiation (transcription) complex with RNA polymerase II (Pol II)
Structure and role of TFIID and other transcription factors (TBP, TAFs)
TFIIB domains for interaction with TFIID/TATA complex
Phosphorylation of CTD of a subunit of Pol II
Formation of pre-initiation complex with Pol I and Pol III
Separate DNA binding and transcription activation domains
Transcription factors and elongation of RNA chains in eukaryotes
Chromatin structure and transcription
Transcription in mitochondria
Transcription of vertebrate mtDNA
Transcription of yeast and plant mtDNA
Transcription in chloroplasts
Elongation arrest vs termination of transcription
The elongation of the transcript may be impeded by (i) 'pause sites', (ii) 'arrest sites' or 'dead ends' and (iii) 'terminators' or 'release sites' (Fig. 32.5). The 'pause sites' induce a temporary reversible block to nucleotide addition. The 'arrest sites' stop elongation, to be resumed only in the presence of elongation factors GreA and GreB (in eukaryotes the corresponding transcription factor is TFIIS described later in this section), which assist in a novel transcript cleavage reaction (Fig. 32.27). The 'release sites' lead to release of RNA and/or RNAP either intrinsically, or upon activation by factors like NusA, Rho, or Tau.

A transcription unit, showing promoter region, start point and terminator; also shown is the role of RNA polymerase with its core enzyme and sigma factor.
Fig. 32.5. A transcription unit, showing promoter region, start point and terminator; also shown is the role of RNA polymerase with its core enzyme and sigma factor.
 
The role of TFIIS in elongation of RNA chain (see text for details).
Fig. 32.27. The role of TFIIS in elongation of RNA chain (see text for details).

Although the nature of DNA sequences causing transcription arrest is not known, the mechanism of transcription arrest and the roles of GreA and GreB in restoring elongation can be explained in the framework of 'inchworm model' described above. The transcription arrest may result when the catalytic site of RNAP is misplaced from the 3' end of growing transcript. This, itself may result, if the 'lagging product site' slipped backward on the template, bringing the catalytic site out of register. Transcript cleavage by GreB would create a new 3' end into the right register, thus restoring elongation. Further, at some template sites, translocation may disturb the placement of catalytic site into the right register, and GreA-induced cleavage of short segments might restore the appropriate register to resume elongation. Thus an elongation barrier may be overcome by RNAP through a 'backup and restart' mechanism.