Mitochondrial DNA, chloroplast DNA and the origins of development in eukaryotic organisms

<p>Abstract</p> <p>Background</p> <p>Several proposals have been made to explain the rise of multicellular life forms. An internal environment can be created and controlled, germ cells can be protected in novel structures, and increased organismal size allows a "division of labor" among cell types. These proposals describe advantages of multicellular versus unicellular organisms at levels of organization at or above the individual cell. I focus on a subsequent phase of evolution, when multicellular organisms initiated the process of development that later became the more complex embryonic development found in animals and plants. The advantage here is realized at the level of the mitochondrion and chloroplast.</p> <p>Hypothesis</p> <p>The extreme instability of DNA in mitochondria and chloroplasts has not been widely appreciated even though it was first reported four decades ago. Here, I show that the evolutionary success of multicellular animals and plants can be traced to the protection of organellar DNA. Three stages are envisioned. <it>Sequestration </it>allowed mitochondria and chloroplasts to be placed in "quiet" germ line cells so that their DNA is not exposed to the oxidative stress produced by these organelles in "active" somatic cells. This advantage then provided <it>Opportunity</it>, a period of time during which novel processes arose for signaling within and between cells and (in animals) for cell-cell recognition molecules to evolve. <it>Development </it>then led to the enormous diversity of animals and plants.</p> <p>Implications</p> <p>The potency of a somatic stem cell is its potential to generate cell types other than itself, and this is a systems property. One of the biochemical properties required for stemness to emerge from a population of cells might be the metabolic quiescence that protects organellar DNA from oxidative stress.</p> <p>Reviewers</p> <p>This article was reviewed by John Logsdon, Arcady Mushegian, and Patrick Forterre.</p

A multiple-method approach reveals a declining amount of chloroplast DNA during development in Arabidopsis

<p>Abstract</p> <p>Background</p> <p>A decline in chloroplast DNA (cpDNA) during leaf maturity has been reported previously for eight plant species, including <it>Arabidopsis thaliana</it>. Recent studies, however, concluded that the amount of cpDNA during leaf development in Arabidopsis remained constant.</p> <p>Results</p> <p>To evaluate alternative hypotheses for these two contradictory observations, we examined cpDNA in Arabidopsis shoot tissues at different times during development using several methods: staining leaf sections as well as individual isolated chloroplasts with 4',6-diamidino-2-phenylindole (DAPI), real-time quantitative PCR with DNA prepared from total tissue as well as from isolated chloroplasts, fluorescence microscopy of ethidium-stained DNA molecules prepared in gel from isolated plastids, and blot-hybridization of restriction-digested total tissue DNA. We observed a developmental decline of about two- to three-fold in mean DNA per chloroplast and two- to five-fold in the fraction of cellular DNA represented by chloroplast DNA.</p> <p>Conclusion</p> <p>Since the two- to five-fold reduction in cpDNA content could not be attributed to an artifact of chloroplast isolation, we conclude that DNA within Arabidopsis chloroplasts is degraded <it>in vivo </it>as leaves mature.</p

RecA maintains the integrity of chloroplast DNA molecules in Arabidopsis

Although our understanding of mechanisms of DNA repair in bacteria and eukaryotic nuclei continues to improve, almost nothing is known about the DNA repair process in plant organelles, especially chloroplasts. Since the RecA protein functions in DNA repair for bacteria, an analogous function may exist for chloroplasts. The effects on chloroplast DNA (cpDNA) structure of two nuclear-encoded, chloroplast-targeted homologues of RecA in Arabidopsis were examined. A homozygous T-DNA insertion mutation in one of these genes (cpRecA) resulted in altered structural forms of cpDNA molecules and a reduced amount of cpDNA, while a similar mutation in the other gene (DRT100) had no effect. Double mutants exhibited a similar phenotype to cprecA single mutants. The cprecA mutants also exhibited an increased amount of single-stranded cpDNA, consistent with impaired RecA function. After four generations, the cprecA mutant plants showed signs of reduced chloroplast function: variegation and necrosis. Double-stranded breaks in cpDNA of wild-type plants caused by ciprofloxacin (an inhibitor of Escherichia coli gyrase, a type II topoisomerase) led to an alteration of cpDNA structure that was similar to that seen in cprecA mutants. It is concluded that the process by which damaged DNA is repaired in bacteria has been retained in their endosymbiotic descendent, the chloroplast

W and Z Boson Production in PbarP Collisions at Sqrt(s)=1.8 TeV

The inclusive cross sections times leptonic branching ratios for W and Z boson production in PbarP collisions at Sqrt(s)=1.8 TeV were measured using the D0 detector at the Fermilab Tevatron collider: Sigma_W*B(W->e, nu) = 2.36 +/- 0.07 +/- 0.13 nb, Sigma_W*B(W->mu,nu) = 2.09 +/- 0.23 +/- 0.11 nb, Sigma_Z*B(Z-> e, e) = 0.218 +/- 0.011 +/- 0.012 nb, Sigma_Z*B(Z->mu,mu) = 0.178 +/- 0.030 +/- 0.009 nb. The first error is the combined statistical and systematic uncertainty, and the second reflects the uncertainty in the luminosity. For the combined electron and muon analyses we find: [Sigma_W*B(W->l,nu)]/[Sigma_Z*B(Z->l,l)] = 10.90 +/- 0.49. Assuming Standard Model couplings, this result is used to determine the width of the W boson: Gamma(W) = 2.044 +/- 0.093 GeV.Comment: 11 pages (including 2 figure pages), in REVTEX. Two PostScript figures are appended in a UUencoded fil

Search for Right-Handed WW Bosons and Heavy W′W^\prime in ppˉp\bar p Collisions at s=\sqrt{s} =1.8 TeV

We report on a search for right-handed $W$ bosons ($W_R$). We used data collected with the D{\O} detector at the Fermilab Tevatron $p\bar p$ collider at $\sqrt{s}=$1.8 TeV to search for $W_R$ decays into an electron and a massive right-handed neutrino $W_R^\pm \to e^\pm N_R$. Using the inclusive electron data, we set mass limits independent of the $N_R$ decay: $m_{W_R}>650$ GeV/c$^2$ and $m_{W_R}>720$ GeV/c$^2$ at the 95% confidence level, valid for $m_{N_R}<{1/2}m_{W_R}$ and $m_{N_R} \ll m_{W_R}$ respectively. The latter also represents a new lower limit on the mass of a heavy left-handed $W$ boson ($W^\prime$) decaying into $e \nu$. In addition, limits on $m_{W_R}$ valid for larger values of the $N_R$ mass are obtained assuming that $N_R$ decays to an electron and two jets.Comment: 15 pages, 5 figures (in UUencoded postscript file which will follow) uses preprint,epsf,eqsecnum,aps,floats,revtex Submitted to Physical Review Letter