Since tRNA secondary structures play a crucial role in RNA maturation from the polycistronic transcripts, it is not clear by what mechanism transcript cleavage would occur at the 3' end of nad5, nad1 and cox1, as these are not flanked by tRNA genes [ 16].
First, standard methods of microarray analysis measure mRNA abundance, not mRNA synthesis or mRNA decay, and, therefore, do not provide any information regarding the mechanisms regulating transcript levels.
The factor that distinguishes between these mechanisms is transcript length.
These may provide clues regarding the mechanisms of transcript localization.
As a possible alternative, a parsimonious model in line with these data could postulate a general orthogonality between the mechanisms controlling transcript levels and translation in mammalian cells.
These studies have the potential to identify the mechanisms controlling transcript levels because the genotype can be considered to be causative, although it may affect gene expression indirectly.
We successfully employed deep sequencing RNA-Seq data in combination with an elaborate bioinformatics strategy in order to identify novel genes, incorrect gene models and mechanisms of transcript processing in the corn anthracnose fungus C. graminicola.
The consequence is an explosion in intron numbers, compensatory evolution of a number of mechanisms of transcript quality control (the nucleus [ 2], nonsense-mediated decay (NMD), ubiquitinylation), and side-effects such as the evolution of linear chromosomes with telomeres and telomerase.
The consequence is an explosion in intron-numbers, compensatory evolution of a number of mechanisms of transcript quality control (the nucleus, Martin & Koonin op. cit)., nonsense-mediated decay (NMD), ubiquitinylation), and side-effects such as the evolution of linear chromosomes with telomeres and telomerase.
We hypothesized that the dramatically different fractions of alternative nucleotides in 5′ UTRs and CDS could be at least partially explained by the dominance of different mechanisms of transcript variability and regulation between domains, namely, ATI in 5′ UTRs and AS in CDS.
Typically, transcriptional control is examined as the main mechanism regulating transcript abundance, however, given the observed down-regulation, a role for mRNA degradation was also considered.
