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Highly Iterated Palindromic Sequences (HIPs) and Their Relationship to DNA Methyltransferases.

Elhai J - Life (Basel) (2015)

Bottom Line: The sequence GCGATCGC (Highly Iterated Palindrome, HIP1) is commonly found in high frequency in cyanobacterial genomes.Taken together, the results point to a role of DNA methylation in the creation or functioning of HIP sites.A model is presented that postulates the existence of a GmeC-dependent mismatch repair system whose activity creates and maintains HIP sequences.

View Article: PubMed Central - PubMed

Affiliation: Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, VA 23284, USA. ElhaiJ@vcu.edu.

ABSTRACT
The sequence GCGATCGC (Highly Iterated Palindrome, HIP1) is commonly found in high frequency in cyanobacterial genomes. An important clue to its function may be the presence of two orphan DNA methyltransferases that recognize internal sequences GATC and CGATCG. An examination of genomes from 97 cyanobacteria, both free-living and obligate symbionts, showed that there are exceptional cases in which HIP1 is at a low frequency or nearly absent. In some of these cases, it appears to have been replaced by a different GC-rich palindromic sequence, alternate HIPs. When HIP1 is at a high frequency, GATC- and CGATCG-specific methyltransferases are generally present in the genome. When an alternate HIP is at high frequency, a methyltransferase specific for that sequence is present. The pattern of 1-nt deviations from HIP1 sequences is biased towards the first and last nucleotides, i.e., those distinguish CGATCG from HIP1. Taken together, the results point to a role of DNA methylation in the creation or functioning of HIP sites. A model is presented that postulates the existence of a GmeC-dependent mismatch repair system whose activity creates and maintains HIP sequences.

No MeSH data available.


Model for the biased creation of new HIP sequences. In each panel, a sequence containing a MTase recognition site (or a near miss) is presumed to have just been replicated. The lower strand is the parental strand and the upper strand is newly synthesized. Pre-existing recognition sites are therefore hemimethylated, with one methylated cytosine (red). Two mutations are shown as taking place during replication. In the left-hand case, the mutation leads to a G lying next to the C at the MTase's methylation site. The C is acted on by the MTase (red blob. Strands with  are then recognized by a hypothetical GmeC-specific nicking enzyme (blue blob; analogous to MutH in E. coli), which nicks the strand opposite the methylation. This allows MutL/MutS to degrade the opposite strand and DNA polymerase to synthesize a new strand using the mutated upper strand as the template. The sequences at the bottom of each panel are those produced by the described mechanism. Sequences in parentheses are special cases (see text). (A) Mutation of nucleotide to the left of CGATCG in a typical cyanobacterium; (B) Mutation of a sequence one off from GrCGyC in Calothrix PCC 7103 (i); (C) Mutation of a sequence one off from rCCGGy in Oscillatoria PCC 10802 (h); (D) Mutation of a sequence one off from GCsGC in Cyanothece PCC 7822 (d). Letters in parentheses refer to symbols in Table 2.
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life-05-00921-f006: Model for the biased creation of new HIP sequences. In each panel, a sequence containing a MTase recognition site (or a near miss) is presumed to have just been replicated. The lower strand is the parental strand and the upper strand is newly synthesized. Pre-existing recognition sites are therefore hemimethylated, with one methylated cytosine (red). Two mutations are shown as taking place during replication. In the left-hand case, the mutation leads to a G lying next to the C at the MTase's methylation site. The C is acted on by the MTase (red blob. Strands with are then recognized by a hypothetical GmeC-specific nicking enzyme (blue blob; analogous to MutH in E. coli), which nicks the strand opposite the methylation. This allows MutL/MutS to degrade the opposite strand and DNA polymerase to synthesize a new strand using the mutated upper strand as the template. The sequences at the bottom of each panel are those produced by the described mechanism. Sequences in parentheses are special cases (see text). (A) Mutation of nucleotide to the left of CGATCG in a typical cyanobacterium; (B) Mutation of a sequence one off from GrCGyC in Calothrix PCC 7103 (i); (C) Mutation of a sequence one off from rCCGGy in Oscillatoria PCC 10802 (h); (D) Mutation of a sequence one off from GCsGC in Cyanothece PCC 7822 (d). Letters in parentheses refer to symbols in Table 2.

Mentions: Figure 6A illustrates the process by which GmeC-dependent MMR might lead to an increase in sequences one off from HIP1. A CGATCG site in a typical cyanobacterium has just been replicated, yielding a parental, methylated strand and a new, unmethylated strand. The panel depicts two cases in which a mutation has occurred during replication just to the left of the CGATCG site. In the left-hand case, the nucleotide has mutated to a G, producing a GmeC site recognized by the postulated GmeC MutH analog. The binding of this protein directs MMR to nick and degrade the opposite strand, thereby preserving the mutation. In contrast, a mutation to any other nucleotide does not produce a GmeC site, and the mismatch is resolved at random (or the mutation is preferentially lost if it happens to lie within ~1000 nt of a distant GmeCGATCG site). As a result, the number of GmeCGATCG sites increases.


Highly Iterated Palindromic Sequences (HIPs) and Their Relationship to DNA Methyltransferases.

Elhai J - Life (Basel) (2015)

Model for the biased creation of new HIP sequences. In each panel, a sequence containing a MTase recognition site (or a near miss) is presumed to have just been replicated. The lower strand is the parental strand and the upper strand is newly synthesized. Pre-existing recognition sites are therefore hemimethylated, with one methylated cytosine (red). Two mutations are shown as taking place during replication. In the left-hand case, the mutation leads to a G lying next to the C at the MTase's methylation site. The C is acted on by the MTase (red blob. Strands with  are then recognized by a hypothetical GmeC-specific nicking enzyme (blue blob; analogous to MutH in E. coli), which nicks the strand opposite the methylation. This allows MutL/MutS to degrade the opposite strand and DNA polymerase to synthesize a new strand using the mutated upper strand as the template. The sequences at the bottom of each panel are those produced by the described mechanism. Sequences in parentheses are special cases (see text). (A) Mutation of nucleotide to the left of CGATCG in a typical cyanobacterium; (B) Mutation of a sequence one off from GrCGyC in Calothrix PCC 7103 (i); (C) Mutation of a sequence one off from rCCGGy in Oscillatoria PCC 10802 (h); (D) Mutation of a sequence one off from GCsGC in Cyanothece PCC 7822 (d). Letters in parentheses refer to symbols in Table 2.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390886&req=5

life-05-00921-f006: Model for the biased creation of new HIP sequences. In each panel, a sequence containing a MTase recognition site (or a near miss) is presumed to have just been replicated. The lower strand is the parental strand and the upper strand is newly synthesized. Pre-existing recognition sites are therefore hemimethylated, with one methylated cytosine (red). Two mutations are shown as taking place during replication. In the left-hand case, the mutation leads to a G lying next to the C at the MTase's methylation site. The C is acted on by the MTase (red blob. Strands with are then recognized by a hypothetical GmeC-specific nicking enzyme (blue blob; analogous to MutH in E. coli), which nicks the strand opposite the methylation. This allows MutL/MutS to degrade the opposite strand and DNA polymerase to synthesize a new strand using the mutated upper strand as the template. The sequences at the bottom of each panel are those produced by the described mechanism. Sequences in parentheses are special cases (see text). (A) Mutation of nucleotide to the left of CGATCG in a typical cyanobacterium; (B) Mutation of a sequence one off from GrCGyC in Calothrix PCC 7103 (i); (C) Mutation of a sequence one off from rCCGGy in Oscillatoria PCC 10802 (h); (D) Mutation of a sequence one off from GCsGC in Cyanothece PCC 7822 (d). Letters in parentheses refer to symbols in Table 2.
Mentions: Figure 6A illustrates the process by which GmeC-dependent MMR might lead to an increase in sequences one off from HIP1. A CGATCG site in a typical cyanobacterium has just been replicated, yielding a parental, methylated strand and a new, unmethylated strand. The panel depicts two cases in which a mutation has occurred during replication just to the left of the CGATCG site. In the left-hand case, the nucleotide has mutated to a G, producing a GmeC site recognized by the postulated GmeC MutH analog. The binding of this protein directs MMR to nick and degrade the opposite strand, thereby preserving the mutation. In contrast, a mutation to any other nucleotide does not produce a GmeC site, and the mismatch is resolved at random (or the mutation is preferentially lost if it happens to lie within ~1000 nt of a distant GmeCGATCG site). As a result, the number of GmeCGATCG sites increases.

Bottom Line: The sequence GCGATCGC (Highly Iterated Palindrome, HIP1) is commonly found in high frequency in cyanobacterial genomes.Taken together, the results point to a role of DNA methylation in the creation or functioning of HIP sites.A model is presented that postulates the existence of a GmeC-dependent mismatch repair system whose activity creates and maintains HIP sequences.

View Article: PubMed Central - PubMed

Affiliation: Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, VA 23284, USA. ElhaiJ@vcu.edu.

ABSTRACT
The sequence GCGATCGC (Highly Iterated Palindrome, HIP1) is commonly found in high frequency in cyanobacterial genomes. An important clue to its function may be the presence of two orphan DNA methyltransferases that recognize internal sequences GATC and CGATCG. An examination of genomes from 97 cyanobacteria, both free-living and obligate symbionts, showed that there are exceptional cases in which HIP1 is at a low frequency or nearly absent. In some of these cases, it appears to have been replaced by a different GC-rich palindromic sequence, alternate HIPs. When HIP1 is at a high frequency, GATC- and CGATCG-specific methyltransferases are generally present in the genome. When an alternate HIP is at high frequency, a methyltransferase specific for that sequence is present. The pattern of 1-nt deviations from HIP1 sequences is biased towards the first and last nucleotides, i.e., those distinguish CGATCG from HIP1. Taken together, the results point to a role of DNA methylation in the creation or functioning of HIP sites. A model is presented that postulates the existence of a GmeC-dependent mismatch repair system whose activity creates and maintains HIP sequences.

No MeSH data available.