Microbial Control of Oceanic Carbon Flux: The Plot Thickens

Farooq Azam

Science, New Series, Vol. 280, No. 5364. (May 1, 1998), pp. 694-696.

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ment of the flieht time and the deflection of the ions enabies their kinetic energy and charge state (X@+) to be determined.

These results confirmed the presence of the highly snipped, very energetic ions ob- served previously for clusters with about 2000 atoms (5) and also provided additional information on the acceleration mecha- nism. In the case of the Coulomb explosion, the energy of repulsion is expected to scale as the square of the ionic charge, whereas, in

the case of hydrodynamic explosions, the energy is purely thermal and scales linearly as the ionic charge and the electron tem- perature. The studies by Lezius et al. of argon clusters that contained typically lo5 atoms indicated that the dominant mechanism was Coulombic but that for xenon clusters that each contained about 10 times more at- oms, lower charge states (q < 6) were Cou- lombic but the majority of the higher charge states (q > 10) were produced by a hydrody- namic expansion. These results for xenon ions of up to q = 30 are summarized in the figure and show the transition in mecha- nism as the ionic charge and the kinetic en- ergy increase. However, the most energetic ions with energies approaching 1 MeV ap- pear to be produced by Coulomb explosion.

Microbial Control of Oceanic Carbon Flux: The Plot Thickens

Farooq Azam

Photosynthesis fixes carbon into organic matter in the ocean. Biological forces then paint intricate flux patterns for carbon in ocean space and in time, as it flows through the food web, becomes stored in the sedi- ments and exchanged with the atmosphere. Predicting how these carbon flux patterns might respond to global change (or to hu- man manipulation) is a primary reason for learning more about the workings of the ocean's carbon cycle. The flux patterns are a result of intricate interactions of a diverse biota with a physically and chemically com- plex pool of organic matter. It now seems that things will get even more complicated before they get simpler. New fundamental findings on the roles of microbes in the fate of organic matter and, recently, on the na- ture of the organic matter itself (14) must be properly assimilated before we can hope to construct ecosystem models to predict the patterns of carbon flux. This impetus could lead to a powerful new synthesis.

What biological forces act on photosyn- thetically produced organic matter in the ocean? Historically, the paradigm has been that essentially all primary production stays within the particle phase (3, it is eaten by herbivores, and the fate of carbon is deter- mined by the "grazing food chain" (see the

The author is at the Scripps Institution of Oceanogra- phy, University of California, La Jolla, CA 92093, USA. E-mail: fazam@ucsd.edu

diagram in the figure below). Little dis- solved organic matter is s~illed for bacteria " to use. It had, therefore, been implicitly as- sumed to be safe to ignore bacteria, proto- zoa, and viruses in studying the fate of or- ganic matter-they were too sparse and not active enough (5). This is now changed (5- 8): Major fluxes of organic matter, often eclipsing the grazing food chain in quantity, move via dissolved organic matter into bac- teria and the "microbial loop" (7, 8) (figure below). Previous methods had missed >99% of microorganisms and had grossly underes- timated their metabolism. Now we know

By the elegant adaptation of a simple ex- perimental technique, Lezius et al. have demonstrated the complexity of the pro- cesses responsible for the dissociation of clusters. Further progress will require more detailed theoretical models to be developed to elucidate further the physical mecha- nisms responsible.

References

1. M. Lezius, S. Dobosz. D. Normand, M. Schmidt, Phys. Rev. Lett. 80, 261 (1998).

2. A. McPherson. B. D. Thompson, A. B. Borisov, K. Boyer. C. K. Rhodes, Nature370, 631 (1994).

3. T. Ditrnire, T. Donnelly. R. W. Falcone, M. D. Perry, Phys. Rev. Lett.,75. 3122 (1995).

4. J. W. G. Tisch et a/., J. Phys. B. Lett. 30. L709 (1997).

5. T. Ditmire eta/., Phys. Rev. A 57, 369 (1998).

from extensive field studies that in most of the ocean, organic matter flux into bacteria is a major pathway; one-half of oceanic pri- mary production on average is channeled via bacteria into the microbial loop (7,8)- a major biological force in the ocean.

Ocean basin-scale biogeochemical stud- ies now routinely quantify organic matter fluxes into bacteria in conjunction with other major flux pathways: grazing food chain, sinking flux, and dissolved organic matter "storage." The fraction of primary production used by bacteria (F,) is highly variable over various time and space scales (7-10). The magnitudes and variability of the fluxes are large enough to cause variabil- ity in flux partitioning between competing pathways (see figure below)-the microbial loop, the grazing food chain, sinking fluxes, and storage of dissolved organic matter (8, 9). Fish production in the eastern Mediter- ranean was diminished by a dominant mi- crobial loop (F, = 0.85) (1 l). In an earlier study (IZ), the richness of the fishery in

0,. CO, other gases

N (ind. uv)

Pollutants Radionuclides

Pathoaens b

The microbial loop: classical version. Modern view of the pelagic food web, emphasizing the microbial loop as a major path for organic matter flux. Competition between the three main flux paths--grazing food chain, microbial loop, and sinking-significantly affects oceanic carbon cycle and productivity. DOM, dissolved organic matter; DMS, dimethylsulfide.

SCIENCE VOL. 280 1 MAY 1998 www.sciencemag.org

Thus, liellavioral and metal~olic re-sponses of bacteria to the complex and het-erogeneous structure of the organic matter field a t the rnicroscale influence ocean ba-sin-scale carhon fluxes in all major path-ways lnicrohial loop, sinking, grazing food chain, carbon storage, and carlion fixation itself. Hon.e\.er, studying such varied influ-ences of bacteria o n organic matter, and their spatial-te~nporalvariations, in piece-~ n e a lfashion bvill only result in a conceptual patch\%-orkwithout a unifying framework or predictive poLver. A unif\-ing theme shoulil derive from applying robust principles of biochemical adaptation in a realistic mi-croenviron~nentalcontext. Biogeochemical varialiility could then be considered as a consequence of adaptive responses to (1nicro)environ111e11talvariations. This ap-proach should also serve as a framebvork to ~ ~ n d e r s t a n dthe maintenance of microliial diversity and to make predictions o n the survival of specific bacterial species, includ-ing human pathogens such as \?brio cholerne, in response to ecosystem perturbations ( 21) . This frame~vork,n.hich includes bacteria-al-gae interactions, should also be relevant to the prediction of algal hlooms, including

toxigenic species. Pon~erfulnen. approaches are enahling us to stud\- ~nicrobialecology, incluiline consortia1 activities, in an ecosvs-ten1 context. N e ~ vtechniques allow mul-tiple interrogatio~ls-phyloge~~y,metallo-lism, gro~vth-at the individual cell level. These ideas and approaches shoulil lead to a synthesis of bacterial a d a ~ t a t i o n ,e\,olution, ecology, anil biogeochemistry, ancl should form a basis for integrating the roles of bac-teria in predictive biogeochemical models.

References and Notes

1 \,VC Chn et ai N a t ~ r e391, 568(1998) 2 F Azar et a1 . M~crobloiEcoi 28 167(1993) 3 F Azam and D C Smlrh, In Part~cleAnaiysls ln

Oceanography S Derers, Ed (Sprnger-Verag, Bern , 1991j. pp 213-236

4 I Ko~keet a / , Nature 345 242(1990)b1 L \i\iels and E D Godberg lbld 353, 342(1991)R A Long and F Azar Aquat Mlcrob Ecoi 10. 2'3 (1996)

5 J Y Steele n r i le Str~ctureof ivlarlne Ecosys-tems (Yarvard Un~v Press Catrbr~dge Pb4A 1974)

6 L R Pomeroy B~osc~ence24 499 (1974).J E t lobbe et a / , Appi Envlron M~crob~oi33 1225 (1977)

7 F Azam et a / , Mar Ecoi Prog Ser 10, 257 (1983)

8 J J Cole et ai 1b1d 43, 1 ('988)J A Fuhrran and F Azatr Mar B ~ o i66 109 (1982).A

Hagstror et a1 Appi Envlron ,Wlcrot?~oi37 805 119791 \ - -,

9 Li \i\i Dl~cklov!and C A Carlson, Aav Mlcrob Ecoi 12 113(1993)

10 h \i\i Duckov! Deep Sea Res 40. 753(1993) 1 1 lu W~llarrs,Sc~ence279, 483(1998). 12 L R Poreroq and D Delbe 1b1d 233 359

(1986) I3 A L Adredge et ai Deep Sea Res 40. 1131

(1993) 14 J G bl~tchelet a i . Appi Envlron M~crobloi61

4436(1995)Y -P Grossa,-tand F Azam paper presented at the Ocean Sclences Pb4eetlng,San Dego CA 9 to ;3February '998

15 h G hoqpe et a1 ,War Ecoi Prog Ser 93 277 (1993)J T Liolbaugh and F Azar , i ~ m n o l Ocearogr 28. 104(1983)

16 E F DeLong et a i , i ~ m n o iOcearogr 38 924 (1993).A,-S Rehnstam et a1 >FEMS,Wlcrob Ecoi 102, 161 (1993).J kdartinez e ta i , Aquat Mlcrob Ecoi 10, 223(1996)

17 h N~ssenet ai . Mar Ecoi Prog Ser 16 155 (1984)G G Geesey and R Y Pb4or1ta,Appi Envlron iLl1cro51oi38 1092(1979)

18 J Stern, personal cornlnunlcat,on 19 D C Smth et a / , Nature 359, 139 (;992)A L

Adredge and C C Gotschak. Cont Sheif Res 10 41 f.1990)

20 D C S r t h et a1 Deeo Sea Res 11 42 75(19951, C1 Passow and A L Alldredge lbld p 99

21 P R Epste~r B~osystems31. 209 (1993).R R Colwsl, Sc~ence274. 2025(1996)

22 I thank Y -P Grossart, R A Lona L B Fandno, X D B~dleD C Sm1;h J T Yoibauoh and F Rasso~~zadeganfor d s c ~ ~ s s o n sand sldgges-tlons Research supported by NSF gran-s NSF OPP96-17045and OPP95-40851

Triplet-Repeat Transcripts: A Role for RNA in Disease

Robert H. Singer

A set of liaftling human diseases-includ-ing myotonic d\-strophy and Huntington's disease-are caused 11\- expansion of a re-peated sequence of three nucleotiiles nrithin almost a dozen genes identified to Ja te ( 1 ) . W i t h each generation, these repeats are rep-licated and the sequence gets longer, even-tually conlprom~singthe function of the gene. T h e effect is dominant-only one of the t ~ oalleles of the gene need lie expanded to result in the full pathology. Furthermore, the severity of the disease can be propor-tional to the length of the repeat expansion.

Unlike most genetic diseases, which are a result of a mutation that Impairs or elimi-nates a gene product, the triplet-repeat dis-eases are likely caused by a "gain of func-tion," in which a nelv f ~ ~ ~ l c t i o narises from the genetic defect. T h e new func t~on1s

The author IS n the Departlnent of Anatotry and Strldc-tura Boogy and Cell Biology, Insttldte for 1:4oecular h4edcne. Albert Ensten College of PLledcne Bronx NY lOr6I USA E - r a rhs~nger@aecomy l ~edld

most easily understood when the expansion of the triplet CAG, which encodes the amino acid glutainine, occurs within the coding frame of a gene and creates a nen7 protein with a pol\-glutanline tract. Hunt-inoton's disease is one exa~nnleof such an expansion and is typical in that it exhihits a central nervous system pathology, as do all the polygl~~tamined~seases.Normal indi-viduals call n-ithstand a f e ~ vrepeats of glutamine a t this position 111 t h e ~ rgenes. As the polyglutamine expands, ho~vever,it ilis-nlnts the ~lrote inand affects celh~larfunc-tions, possibly due to the high charge den-sity of the expandi~lgrepeat. T h e new, gain-of-function protein can wreak havoc 011 cel-lular processes such as nuclear export, RNA and D N A hindino, or ~ n e ~ n b r a n et r a n s ~ o r t .

Expa~ls io~lsof these triplet repeats can also occur outside the coding reglon, but in these instances nelv proteins are not pro-duced. LYi~th~nthis group of disorders, myotonic dystrophy is a particular curiosity. In this disease, the expansloll occurs in the

~ ~ n t r a n s l a t e ~ lregion of the transcript, after nrote i~lcodine has occurred, and can ill--crease the 1llRN.A hy 6 kilobases or more. As this expa~ l s io~ lgets progressively larger in one of the alleles, the resulting pathology of the disease becomes ~ ~ r o ~ ~ o r t i o ~ ~ a t e l vmore

L .

severe. This behavior begs for a new moclel of molecular cytopathology. Such a model is provided bv Ph i l i~x .Timchenko. and Coo-per o n page 737 of this issue. They propose that the gain of f ~ ~ n c t i o nin m\-otonic dvs-

u

trophy is a t least in part a result of disrupted activity of a CUG-binding protein induced hy the repeats in the R N A , which prevents it from doing its normal joh of splicing a cer-tain family of penes., -

T h e ne\v proposal is not the first; various nlodels have been readily forthcoming since the first description of these d~seases.None has lieen sufficient to explain the molecular etioloey. T h e es~7ansionmost likely occurs-,

initially in the germ cells or early emhryos, \\,here the D N A polymerase may "stutter" o n the repeats and, in doing so, expand them. Some models rely on DNA-based mechanisms to explain the pathology of these diseases-changes in chrolnatin orga-nization because of n~~c leosome~ ~ o s ~ t i o n ~ n e .

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stalling of the R N A polymerase, or suppres-s1o11of other genes nearly. But these models cannot exnlain the trans-dominant effect of the allele, the effect of one abnorlnal gene 011the functioning of the \vhole cell.

A ~ i o t h e rD N A rneclia~lls~llis possible.

696 SCIENCE VOL 1SL7 1 \ I . i U 1998 n.~v~v.sciencem