diff --git a/content/3.defense-systems/abid.md b/content/3.defense-systems/abid.md index c383291c2d90aa06e099af64ddab822ee2e6958f..2844485cd00c8238f6925ef53a6348c1e1aa6e34 100644 --- a/content/3.defense-systems/abid.md +++ b/content/3.defense-systems/abid.md @@ -23,11 +23,12 @@ relevantAbstracts: ## Description -AbiD is a single gene system system discovered in may 1995 in the plasmid pBF61 of *Lactococcus lactis* :ref{doi=10.1128/aem.61.5.2023-2026.1995}. An homologs of AbiD, named AbiD1 was discovered in july 1995 :ref{doi=10.1128/jb.177.13.3818-3823.1995}. +AbiD is a single gene system system discovered in May 1995 in the plasmid pBF61 of *Lactococcus lactis* :ref{doi=10.1128/aem.61.5.2023-2026.1995}. An homolog of AbiD, named AbiD1 was discovered in July 1995 :ref{doi=10.1128/jb.177.13.3818-3823.1995}. -AbiD is one of the so-called "Abi" systems for "Abortive infection" discovered in the 90's in research related to the dairy industry :ref{doi=10.1016/j.mib.2005.06.006}. AbiR is classified as possible abortive infection in :ref{doi=10.1016/j.mib.2023.102312}. +AbiD is one of the so-called "Abi" systems for "Abortive infection" discovered in the 90's in research related to the dairy industry :ref{doi=10.1016/j.mib.2005.06.006}. AbiR is classified as a possible abortive infection in :ref{doi=10.1016/j.mib.2023.102312}. + +This antiphage defense system is very close to AbiD1 and AbiF :ref{doi=10.1128/aem.61.12.4321-4328.1995} and is categorized as the same system. Furthermore, AbiD is also detected as the [Abi2](/defense-systems/abi2) system. -This antiphage defense system is very close to AbiD1 and AbiF :ref{doi=10.1128/aem.61.12.4321-4328.1995} and are categorized as the same system. Furtheremore, AbiD is also detected as the [Abi2](/defense-systems/abi2) system. ### Molecular mechanism For AbiD1 :ref{doi=10.1128/jb.177.13.3824-3829.1995} ([AAA79209](https://www.ncbi.nlm.nih.gov/protein/AAA79209)), the expression of the protein is toxic to the bacteria and is therefore highly regulated. Expression of the protein is triggered by the orf1 of phage bIL66 which results in inhibition of the phage RuvC-like endonuclease activity and stops phage multiplication.