Literature summary for 4.6.1.16 extracted from

Gibb, E.A.; Edgell, D.R.
Better late than early: delayed translation of intron-encoded endonuclease I-TevI is required for efficient splicing of its host group I intron (2010), Mol. Microbiol., 78, 35-46.

Search for more literature for 4.6.1.16

Organism

Organism	UniProt	Comment	Textmining
Tequatrovirus T4	-	-	-

Synonyms

Synonyms	Comment	Organism
homing endonuclease	-	Tequatrovirus T4
I-TevI	-	Tequatrovirus T4
intron-encoded endonuclease	-	Tequatrovirus T4

General Information

General Information	Comment	Organism
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	Tequatrovirus T4
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	Tequatrovirus T4

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Release 2023.1 (January 2023)