Change names for different systems + Add new systems + Remove double titles

content/2.defense-systems/dmdde.md

@@ -4,10 +4,9 @@ tableColumns:
     article:
       doi: 10.1038/s41586-022-04546-y
       abstract: |
-        Horizontal gene transfer can trigger rapid shifts in bacterial evolution. Driven by a variety of mobile genetic elements—in particular bacteriophages and plasmids—the ability to share genes within and across species underpins the exceptional adaptability of bacteria. Nevertheless, invasive mobile genetic elements can also present grave risks to the host; bacteria have therefore evolved a vast array of defences against these elements1. Here we identify two plasmid defence systems conserved in the Vibrio cholerae El Tor strains responsible for the ongoing seventh cholera pandemic2–4. These systems, termed DdmABC and DdmDE, are encoded on two major pathogenicity islands that are a hallmark of current pandemic strains. We show that the modules cooperate to rapidly eliminate small multicopy plasmids by degradation. Moreover, the DdmABC system is widespread and can defend against bacteriophage infection by triggering cell suicide (abortive infection, or Abi). Notably, we go on to show that, through an Abi-like mechanism, DdmABC increases the burden of large low-copy-number conjugative plasmids, including a broad-host IncC multidrug resistance plasmid, which creates a fitness disadvantage that counterselects against plasmid-carrying cells. Our results answer the long-standing question of why plasmids, although abundant in environmental strains, are rare in pandemic strains; have implications for understanding the dissemination of antibiotic resistance plasmids; and provide insights into how the interplay between two defence systems has shaped the evolution of the most successful lineage of pandemic V. cholerae.
+        Horizontal gene transfer can trigger rapid shifts in bacterial evolution. Driven by a variety of mobile genetic elements—in particular bacteriophages and plasmids—the ability to share genes within and across species underpins the exceptional adaptability of bacteria. Nevertheless, invasive mobile genetic elements can also present grave risks to the host; bacteria have therefore evolved a vast array of defences against these elements1. Here we identify two plasmid defence systems conserved in the Vibrio cholerae El Tor strains responsible for the ongoing seventh cholera pandemic2-4. These systems, termed DdmABC and DdmDE, are encoded on two major pathogenicity islands that are a hallmark of current pandemic strains. We show that the modules cooperate to rapidly eliminate small multicopy plasmids by degradation. Moreover, the DdmABC system is widespread and can defend against bacteriophage infection by triggering cell suicide (abortive infection, or Abi). Notably, we go on to show that, through an Abi-like mechanism, DdmABC increases the burden of large low-copy-number conjugative plasmids, including a broad-host IncC multidrug resistance plasmid, which creates a fitness disadvantage that counterselects against plasmid-carrying cells. Our results answer the long-standing question of why plasmids, although abundant in environmental strains, are rare in pandemic strains; have implications for understanding the dissemination of antibiotic resistance plasmids; and provide insights into how the interplay between two defence systems has shaped the evolution of the most successful lineage of pandemic V. cholerae.
 ---
 
-# DmdDE
 # DmdDE
 ## Example of genomic structure
 

content/2.defense-systems/dnd.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Nucleic acid degrading
 ---
 
-# Dnd
 # Dnd
 ## Example of genomic structure
 

content/2.defense-systems/dodola.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Dodola
 # Dodola
 ## Example of genomic structure
 

content/2.defense-systems/dpd.md

@@ -4,10 +4,9 @@ tableColumns:
     article:
       doi: 10.1073/pnas.1518570113
       abstract: |
-        The discovery of ?20-kb gene clusters containing a family of paralogs of tRNA guanosine transglycosylase genes, called tgtA5, alongside 7-cyano-7-deazaguanine (preQ0) synthesis and DNA metabolism genes, led to the hypothesis that 7-deazaguanine derivatives are inserted in DNA. This was established by detecting 2’-deoxy-preQ0 and 2’-deoxy-7-amido-7-deazaguanosine in enzymatic hydrolysates of DNA extracted from the pathogenic, Gram-negative bacteria Salmonella enterica serovar Montevideo. These modifications were absent in the closely related S. enterica serovar Typhimurium LT2 and from a mutant of S. Montevideo, each lacking the gene cluster. This led us to rename the genes of the S. Montevideo cluster as dpdA-K for 7-deazapurine in DNA. Similar gene clusters were analyzed in ?150 phylogenetically diverse bacteria, and the modifications were detected in DNA from other organisms containing these clusters, including Kineococcus radiotolerans, Comamonas testosteroni, and Sphingopyxis alaskensis. Comparative genomic analysis shows that, in Enterobacteriaceae, the cluster is a genomic island integrated at the leuX locus, and the phylogenetic analysis of the TgtA5 family is consistent with widespread horizontal gene transfer. Comparison of transformation efficiencies of modified or unmodified plasmids into isogenic S. Montevideo strains containing or lacking the cluster strongly suggests a restriction–modification role for the cluster in Enterobacteriaceae. Another preQ0 derivative, 2’-deoxy-7-formamidino-7-deazaguanosine, was found in the Escherichia coli bacteriophage 9g, as predicted from the presence of homologs of genes involved in the synthesis of the archaeosine tRNA modification. These results illustrate a deep and unexpected evolutionary connection between DNA and tRNA metabolism.
+        The discovery of ?20-kb gene clusters containing a family of paralogs of tRNA guanosine transglycosylase genes, called tgtA5, alongside 7-cyano-7-deazaguanine (preQ0) synthesis and DNA metabolism genes, led to the hypothesis that 7-deazaguanine derivatives are inserted in DNA. This was established by detecting 2’-deoxy-preQ0 and 2’-deoxy-7-amido-7-deazaguanosine in enzymatic hydrolysates of DNA extracted from the pathogenic, Gram-negative bacteria Salmonella enterica serovar Montevideo. These modifications were absent in the closely related S. enterica serovar Typhimurium LT2 and from a mutant of S. Montevideo, each lacking the gene cluster. This led us to rename the genes of the S. Montevideo cluster as dpdA-K for 7-deazapurine in DNA. Similar gene clusters were analyzed in ?150 phylogenetically diverse bacteria, and the modifications were detected in DNA from other organisms containing these clusters, including Kineococcus radiotolerans, Comamonas testosteroni, and Sphingopyxis alaskensis. Comparative genomic analysis shows that, in Enterobacteriaceae, the cluster is a genomic island integrated at the leuX locus, and the phylogenetic analysis of the TgtA5 family is consistent with widespread horizontal gene transfer. Comparison of transformation efficiencies of modified or unmodified plasmids into isogenic S. Montevideo strains containing or lacking the cluster strongly suggests a restriction-modification role for the cluster in Enterobacteriaceae. Another preQ0 derivative, 2’-deoxy-7-formamidino-7-deazaguanosine, was found in the Escherichia coli bacteriophage 9g, as predicted from the presence of homologs of genes involved in the synthesis of the archaeosine tRNA modification. These results illustrate a deep and unexpected evolutionary connection between DNA and tRNA metabolism.
 ---
 
-# Dpd
 # Dpd
 ## Example of genomic structure
 

content/2.defense-systems/drt.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# DRT
 # DRT
 ## Example of genomic structure
 

content/2.defense-systems/druantia.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Druantia
 # Druantia
 ## Example of genomic structure
 

content/2.defense-systems/dsr.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Nucleotide modifying
 ---
 
-# Dsr
 # Dsr
 ## Example of genomic structure
 

content/2.defense-systems/eleos.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Eleos
 # Eleos
 The Eleos system was previously described as the Dynamins-like system in (Millman et al, 2022).
 

content/2.defense-systems/fs_giy_yig.md

+---
+title: FS_GIY_YIG
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_GIY_YIG
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/fs_hepn_tm.md

+---
+title: FS_HEPN_TM
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_HEPN_TM
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/fs_hp.md

+---
+title: FS_HP
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_HP
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/fs_hp_sdh_sah.md

+---
+title: FS_HP_SDH_sah
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_HP_SDH_sah
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/fs_hsdr_like.md

+---
+title: FS_HsdR_like
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_HsdR_like
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/fs_sma.md

+---
+title: FS_Sma
+tableColumns:
+    article:
+      doi: 10.1016/j.cell.2022.07.014
+      abstract: |
+        Bacteria encode sophisticated anti-phage systems that are diverse and versatile and display high genetic mobility. How this variability and mobility occurs remains largely unknown. Here, we demonstrate that a widespread family of pathogenicity islands, the phage-inducible chromosomal islands (PICIs), carry an impressive arsenal of defense mechanisms, which can be disseminated intra- and inter-generically by helper phages. These defense systems provide broad immunity, blocking not only phage reproduction, but also plasmid and non-cognate PICI transfer. Our results demonstrate that phages can mobilize PICI-encoded immunity systems to use them against other mobile genetic elements, which compete with the phages for the same bacterial hosts. Therefore, despite the cost, mobilization of PICIs may be beneficial for phages, PICIs, and bacteria in nature. Our results suggest that PICIs are important players controlling horizontal gene transfer and that PICIs and phages establish mutualistic interactions that drive bacterial ecology and evolution.
+---
+
+# FS_Sma
+
+## To do 
+
+## Relevant abstract
+::article-doi-list
+---
+items:
+    - doi: 10.1016/j.cell.2022.07.014
+
+---
+::

content/2.defense-systems/gabija.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Degrading nucleic acids
 ---
 
-# Gabija
 # Gabija
 ## Description
 

content/2.defense-systems/gao_ape.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Gao_Ape
 # Gao_Ape
 ## Example of genomic structure
 

content/2.defense-systems/gao_her.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Gao_Her
 # Gao_Her
 ## Example of genomic structure
 

content/2.defense-systems/gao_hhe.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Gao_Hhe
 # Gao_Hhe
 ## Example of genomic structure
 

content/2.defense-systems/gao_iet.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Gao_Iet
 # Gao_Iet
 ## Example of genomic structure
 

content/2.defense-systems/gao_mza.md

@@ -10,7 +10,6 @@ tableColumns:
     Effector: Unknown
 ---
 
-# Gao_Mza
 # Gao_Mza
 ## Example of genomic structure