EC Number   |
General Information |
Reference |
|---|
   4.6.1.16 | evolution |
in Archaea, three types of splicing endonuclease are produced, homotetrameric: alpha4, homodimeric: alpha2, and heterotetrameric: (alphabeta)2. epsilon2 endonuclease represents a fourth type: epsilon2. The presence of an epsilon2 endonuclease in an archaeon deeply branched within Euryarchaeota represents an example of the coevolution of tRNA and their processing enzymes. The ancestral alpha4 endonuclease is assumed to have undergone two independent gene duplication events giving rise to alpha2 and (alphabeta)2 architecture via subfunctionalization, while most of the (alphabeta)2 endonucleases and korarchaeal a2 endonuclease have acquired extra insertion sequences that interact with BHB motif to broaden their substrate specificity. Transition of splicing endonuclease from alpha4 to epsilon2 type, overview |
718175 |
| 4.6.1.16 | evolution |
the crenarchaeal heterotetrameric EndAs can be further classified into two subfamilies based on the size of the structural subunit. Subfamily A possesses a structural subunit similar in size to the catalytic subunit, whereas subfamily B possesses a structural subunit significantly smaller than the catalytic subunit |
717994 |
| 4.6.1.16 | malfunction |
deleted key control elements to deregulate I-TevI expression at early and middle times post T4 infection. Deregulation of I-TevI, or of a catalytically inactive variant, generates a thymidine-dependent phenotype that is caused by a reduction in td intron splicing, deregulated I-TevI expression results in defective td intron splicing and overproduction of a truncated thymidylate synthase protein. Prematurely terminating I-TevI translation restores td splicing, full-length TS synthesis, and rescues the thymidine-dependent phenotype, overview |
718130 |
| 4.6.1.16 | malfunction |
epleting HSPC117 by RNA interference abolishes interstrand ligation and impaires processing of pre-tRNA transcripts into mature tRNA in cell extracts |
730963 |
| 4.6.1.16 | malfunction |
mutations in human EndA cause neurological disorders including pontocerebellar hypoplasia and progressive microcephaly |
750620 |
| 4.6.1.16 | more |
APE-EndA possesses a Crenarchaea specific loop, which is responsible for the broad substrate specificity of APE-EndA. Lys44 in CSL functions as the RNA recognition site |
718174 |
| 4.6.1.16 | more |
EndA from Aeropyrum pernix also possesses an extra loop region that is characteristic of crenarchaeal EndAs, the conserved lysine residue Lys44 in the loop is important for endonuclease activity, substrate docking modeling, overview |
717994 |
| 4.6.1.16 | more |
introduction of the Crenarchaea specific loop, CSL, eg.e from Aeropyrum pernix EndA, into AFU-EndA enhances its intron-cleaving activity irrespective of the position or motif of the intron |
718174 |
| 4.6.1.16 | physiological function |
EndA function is required for brain development in humans. Human EndA complex (TSen2, TSen15, TSen34, and TSen54) cleaves introns from pre-tRNAs, and the TSen2 subunit is involved in pre-mRNA'3 end formation |
750620 |
| 4.6.1.16 | physiological function |
the td group I intron interrupting the thymidylate synthase gene of phage T4 is a mobile intron that encodes the homing endonuclease I-TevI. Efficient RNA splicing of the intron is required to restore function of the thymidylate synthase gene, while expression of I-TevI from within the intron is required to initiate intron mobility. Stringent translational control of I-TevI evolved to prevent the ribosome from disrupting key structural elements of the td intron that are required for splicing and thymidylate synthase function at early and middle times post T4 infection |
718130 |
