From 6b58c03cc27a0f91fac3a0488738d502d173366a Mon Sep 17 00:00:00 2001
From: ftesson <florian.tesson@pasteur.fr>
Date: Tue, 16 Jan 2024 16:26:41 +0100
Subject: [PATCH] change ref add figure

---
 content/3.defense-systems/rm.md         |  13 +++++++++----
 public/rm/Figure_1_Tock_Dryden_2005.png | Bin 0 -> 11086 bytes
 2 files changed, 9 insertions(+), 4 deletions(-)
 create mode 100644 public/rm/Figure_1_Tock_Dryden_2005.png

diff --git a/content/3.defense-systems/rm.md b/content/3.defense-systems/rm.md
index 2626cb73..7ac19141 100644
--- a/content/3.defense-systems/rm.md
+++ b/content/3.defense-systems/rm.md
@@ -5,7 +5,7 @@ tableColumns:
     article:
       doi: 10.1016/j.mib.2005.06.003
       abstract: |
-        The rexA and rexB genes of bacteriophage lambda encode a two-component system that aborts lytic growth of bacterial viruses. Rex exclusion is characterized by termination of macromolecular synthesis, loss of active transport, the hydrolysis of ATP, and cell death. By analogy to colicins E1 and K, these results can be explained by depolarization of the cytoplasmic membrane. We have fractionated cells to determine the intracellular location of the RexB protein and made RexB-alkaline phosphatase fusions to analyze its membrane topology. The RexB protein appears to be a polytopic transmembrane protein. We suggest that RexB proteins form ion channels that, in response to lytic growth of bacteriophages, depolarize the cytoplasmic membrane. The Rex system requires a mechanism to prevent lambda itself from being excluded during lytic growth. We have determined that overexpression of RexB in lambda lysogens prevents the exclusion of both T4 rII mutants and lambda ren mutants. We suspect that overexpression of RexB is the basis for preventing self-exclusion following the induction of a lambda lysogen and that RexB overexpression is accomplished through transcriptional regulation.
+        The phenomena of prokaryotic restriction and modification, as well as anti-restriction, were first discovered five decades ago but have yielded only gradually to rigorous analysis. Work presented at the 5th New England Biolabs Meeting on Restriction-Modification (available on REBASE, http://www.rebase.com) and several recently published genetic, biochemical and biophysical analyses indicate that these fields continue to contribute significantly to basic science. Recently, there have been several studies that have shed light on the still developing field of restriction-modification and on the newly re-emerging field of anti-restriction.
     Sensor: Detecting invading nucleic acid
     Activator: Direct
     Effector: Nucleic acid degrading
@@ -25,8 +25,13 @@ Restriction modification systems are the most abundant antiphage systems. They a
 https://en.wikipedia.org/wiki/Restriction_modification_system
 
 ## Molecular Mechanisms
-Several reviews detail the molecular mechanisms of restriction modification systems. For example in :ref{doi=10.1016/j.mib.2005.06.003} 
-*"Bacterial restriction-modification (R-M) systems function as prokaryotic immune systems that attack foreign DNA entering the cell [1]. Typically, R-M systems have enzymes responsible for two opposing activities: a restriction endonuclease (REase) that recognizes a specific DNA sequence for cleavage and a cognate methyltransferase (MTase) that confers protection from cleavage by methylation of adenine or cytosine bases within the same recognition sequence. REases recognize ‘non-self’ DNA (Figure 1), such as that of phage and plasmids, by its lack of characteristic modification within specific recognition sites [2]. Foreign DNA is then inactivated by endonucleolytic cleavage. Generally, methylation of a specific cytosine or adenine within the recognition sequence confers protection from restriction. Host DNA is normally methylated by the MTase following replication, whereas invading non-self DNA is not."*
+Several reviews detail the molecular mechanisms of restriction modification systems. For example in :ref{doi=10.1016/j.mib.2005.06.003}:
+
+*"Bacterial restriction-modification (R-M) systems function as prokaryotic immune systems that attack foreign DNA entering the cell :ref{doi=10.1128/jb.65.2.113-121.1953}. Typically, R-M systems have enzymes responsible for two opposing activities: a restriction endonuclease (REase) that recognizes a specific DNA sequence for cleavage and a cognate methyltransferase (MTase) that confers protection from cleavage by methylation of adenine or cytosine bases within the same recognition sequence. REases recognize ‘non-self’ DNA (Figure 1), such as that of phage and plasmids, by its lack of characteristic modification within specific recognition sites :ref{doi=10.1093/nar/29.18.3705}. Foreign DNA is then inactivated by endonucleolytic cleavage. Generally, methylation of a specific cytosine or adenine within the recognition sequence confers protection from restriction. Host DNA is normally methylated by the MTase following replication, whereas invading non-self DNA is not."*
+
+![Figure 1](/rm/Figure_1_Tock_Dryden_2005.png){max-width=750px}
+
+Figure 1. The function of R-M systems, as illustrated by Type I R-M enzymes. From :ref{doi=10.1016/j.mib.2005.06.003}.
 
 
 ## Example of genomic structure
@@ -70,7 +75,7 @@ Proportion of genome encoding the RM system for the 14 phyla with more than 50 g
 
 ### Experimentaly determined structure
 
-Many structure for the different types of restriction-modification system are available on the [protein data bank](https://www.rcsb.org/).
+Many structure for the different types of restriction-modification system are available on the [Protein Data Bank](https://www.rcsb.org/).
 
 ### RM
 #### Restriction modification Type I Prr
diff --git a/public/rm/Figure_1_Tock_Dryden_2005.png b/public/rm/Figure_1_Tock_Dryden_2005.png
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-- 
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