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DNA evolutionModerator: BioTeam
9 posts • Page 1 of 1
DNA evolutionWhy is DNA double stranded? The answer is - IT GIVES STABILITY. But what kind of stability? Is this a satiesfactory explanation to the changeover from sDNA to dDNA ? What do U think?
hsg
Structural stability
If sDNA loses a base sequence there is no way to find that sequence. Whereas if a dDNA loses a base, the complementary sequence can be found because there's one complementary base. Ideally, if an organism evolves a quadruple redundant DNA structure, it would be able to withstand ageing, radiation etc...
Does this double stranded form help conserve the genetic material ? I think, yes, & this wud have been important pt. in earlier environment .. & what about RNA to DNA change over ? Is there any special benefit of DNA over RNA ?
DNA stores the information...RNA communicates it. DNA can hold more information due to its larger size, and RNA can communicate better due to its smaller size.
Thanks.
By saying RNA to DNA change over I mean appearance of T instead of U in the genetic material.So, i want to know if there are any advantages of T over U..... hrushikesh
H-bonding???I don't know. A possibility is that RNA has a 4' OH group. This group should be both more reactive than the 4' H in DNA as well as a source of hydrogen bonding effects.
-Yes, It is also a stabilizing factor. Thanx . But,-- Sugars in -NAs don't participate in H-bonding. hrushikesh
See this: This article from Virology Journal (http://www.virologyj.com/home) might be of interest to the readership as it (among other things) describes a mechanism that enables protein information to modify RNA information, and is a mechanism of Larmarkian inheritance. The author makes it clear that it remains consistent with Darwinian selection. It also suggest potential weaknesses in viral replication that might be exploited. Hepatitis C (HCV), hepatitis B (HBV), the human immunodeficiency viruses (HIV), and other viruses that replicate via RNA intermediaries, cause an enormous burden of disease and premature death worldwide. These viruses circulate within infected hosts as vast populations of closely related, but genetically diverse, molecules known as "quasispecies". The mechanism(s) by which this extreme genetic and antigenic diversity is stably maintained are unclear, but are fundamental to understanding viral persistence and pathobiology. The persistence of HCV, an RNA virus, is especially problematic and HCV stability, maintained despite rapid genomic mutation, is highly paradoxical. This paper presents the hypothesis, and evidence, that viruses capable of persistent infection autoregulate replication and the likely mechanism mediating autoregulation--Replicative Homeostasis--is described. Replicative homeostasis causes formation of stable, but highly reactive, equilibria that drive quasispecies expansion and generates escape mutation. Replicative homeostasis explains both viral kinetics and the enigma of RNA quasispecies stability and provides a rational, mechanistic basis for all observed viral behaviours and host responses. More importantly, this paradigm has specific therapeutic implication and defines, precisely, new approaches to antiviral therapy. Replicative homeostasis may also modulate cellular gene expression.
9 posts • Page 1 of 1
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