Rob Mellor: Jump to research results about:
I come from a very working-class background in industrial Huddersfield (Ay lad, ther's trubble up a t'mill), but after a not-very-promising childhood managed to win a scholarship to the Queen Elizabeth the First (public school), which resulted in me being given a whole bunch of "O" and "A" level certificates.
I then studied cytogenetics (as molecular biology was called then) and computing at University of Newcastle-upon-Tyne and graduated from there at the age of 19 (although because 2 year degrees are not allowed, I had to wait another year to get the certificate). After jobbing around in Glasgow and Liverpool, I joined Mike Lords research group at the University of Bradford in 1976, doing sub-cellular fractionation studies. We worked on germinating fat-storing seeds, because their cells have no central vacuole, meaning that the fractions are much cleaner than those from cells with vacuoles. I worked on lipid-linked intermediates in the glycosylation of proteins. We saw that core glycosylation in plants is similar to that in animals (although peripheral glycosylation can be very different). This work was largely confirmed by Kagawa and González, 1981, R N Trelease, 1984 and González, 1986. Then I moved to the University of Dundee working on Azolla, for two years and my findings have since been independently substantiated (Ladha, J. K. & Watanabe, I. 1984: Antigenic Analysis of Anabaena azollae and the role of lectin in the Azolla-anabaena symbiosis, New Phytol., 98, 295-300). At Dundee, thanks largely to Janet Sprent, I became interested in N-fixation and in Rhizobial root nodules.
When I was 26 I got my first "real job" at the University of Marburg. BRD (and afterwards a more senior position at the University of Basel, Switzerland) and must admit that Germany in the early/mid 80’s was a great place. As far as science went there were a few things that had to be ironed out. Firstly, legume root nodule cells are filled with Rhizobial bacteria, each of which is surrounded by a membrane envelope called the peri-bacteroid membrane. At that time it was thought that the peri-bacteroid membrane was simply involuted plasma membrane. I didn’t really believe this, and could check it out, since the lack of a central vacuole means that these cells can easily be fractionated. This detailed detective work (click here for some details) earned me the unofficial nickname of "the Columbo of Rhizobium". After a couple of years of painstaking minute work, also involving checking where others had made mistakes (see e.g. Mellor, R.B. and D. Werner 1986: The fractionation of Glycine max root nodule cells: A methodological overview. Endocyt. C. Res., 3, 317-336), I was able to prove that this membrane was a new type of membrane and that the membrane-enclosed bacteroids in fact represented a new type of organelle (and had nothing to do with the plasma-membrane), which had taken over the lysosomal functions in these cells, analogous to the role of protein bodies in seeds (Mellor, R.B.: Bacteroids in the Rhizobium-legume symbiosis inhabit a plant internal lytic compartment: Implications for other microbial endosymbioses. J Exp. Bot., 40, 831-839 (1989).). In particular my findings, published in 1986, that the ATP-ase in the peribacteroid membrane was not the plasma-membrane ATP-ase, was generally pilloried until confirmed by a series of publications a decade later (e.g. Campos et al. 1996. Localization of plasma membrane H+-ATPase in nodules of Phaseolus vulgaris L. Plant Molecular Biology, 32, 1043-1053).
Initially greeted by scepticism, my "symbiosome=lysosome theory" is now generally accepted. This includes the initial disbelief in my 1990 findings that the plant expresses novel proteins in both mycorrhizas and nodules, and that some of these are common to both symbioses (confirmed in Manhej et al (2004). MPMI, 17, 1063-1077). Not waiting for the skeptics to catch up, I was able to build on this by postulating (Mellor, R.B.: The nodulation of legumes. (1996). DSR Forlag, Copenhagen. ISBN: 87-7432-466-7) that in symbioses generally, the micro-symbiont and the macro-symbiont share their lytic / vacuolar compartments (I call this the "unified vacuole theory").
However this was not the only area I worked on. Two other major research themes originated from my curiosity:
As far as trehalose is concerned, my work pointed to that root nodules may be under water stress. Thus root nodules can function as an "early warning indicator" for plants suffering additional drought stress (Mellor, R.B. (1992): Is trehalose a symbiotic determinant in symbioses between higher plants and micro-organisms? Symbiosis, 12, 113-129) and this may explain why nodulated plants have a higher drought-tolerance than non-nodulated plants (Farias-Rodrigues, R., R.B. Mellor, C. Arias and J.J. Pena-Cabriales (1998): Trehalose accumulation in several cultivars of common bean (Phaseolus vulgaris L) and its correlation to drought stress. Physiol. Plant., 102, 353-359.).
If you asked the question "how does the plant distinguish between symbiotic and pathogenic infections" back in 1983, then the answer would be basically about nutrition: that symbiotic plants are healthier and that this suppresses plant defence responses – the plant equivalent of an immune response. I did not believe this because the differences in response occurred much earlier than any nutritional effect. So in 1984 we set about measuring defence responses in nodules infected with different Rhizobial mutants (Werner, D., R.B. Mellor, M.G. Hahn and H. Grisebach (1985): Soybean root response to symbiotic infection: Glyceollin accumulation in an ineffective type of nodule with an early loss of the peribacteroid membrane. Z. Naturforsch., 40, 171-181.)
Many publications later it became obvious that the Rhizobia have nod-genes, and that these genes are responsible for producing different nod-factors (lipo-chitin molecules) and that amongst their many effects was that they can provoke plant defence responses, so that it was essential that these genes were switched off (by molecules called "nodoffs") after infection, or that symbiosis could not take place (Mellor, R.B. and D.B. Collinge (1995): A simple model based on known plant defence reactions is sufficient to explain most aspects of nodulation. J. Exp. Bot., 46, 1-18). This convincing model won general acclaim and indeed it was later reprinted as the year’s number one most important publication.
Years at the cutting edge had taken their toll. Amusing incidents include that in late 1987 I sent in a grant application to study the "symbiosome=lysosome" theory more. One reviewer expressed their opinion quite succinctly "Mellor is a crackpot and does not deserve funding"! Only 6 years later I wrote a review article stressing the lytic nature of the symbiosome and was rewarded with an initial rejection because "the lytic nature of the symbiosome is a well-established and understood fact, there is nothing new in this". Sometimes you just can’t win :o) On the other hand I met a whole load of really great people, in particular the "Good Guys", wonderful unselfish colleagues and brilliant scientists, including; Nick Brewin, Bill Broughton, Frans deBruijn, Peter Gresshoff, Hauke Hennecke, Juan-Jose Pena-Cabriales, Don Phillips, Andrea Schubert & Desh Pal Verma.
So I put Rhizobium on the "back boiler" and was headhunted by a spin-off from the Max-Planck Institute in Göttingen and had a great time not only working with technology transfer but also applying science. One example was the system I invented and patented to power immobilized oxido-reductase enzymes and co-factors using electrical power out of a domestic socket (Mellor, R.B., J. Ronnenberg, W.H. Campbell and S. Diekmann (1992): Reduction of nitrate and nitrite in water by immobilized enzymes. Nature, 355, 717-719). But Germany was not the same as I remembered it from a decade before and I left for Copenhagen to re-group and use my newly found entrepreneurial spirit.
|In Denmark I shed one of my major illusions about life: That humans work together according to unspoken but noble goals, following an intrinsic path to rational, scientific enlightenment and justice, resisting error by collegial co-operation and moving towards a true understanding of the universe we live in. My philosophical transition from the open 1970s meritocratic UK, to an academic environment consisting of despots, petty back-stabbing, rampant selfishmess and nepotism, took several years, but I slowly adjusted from asking high academics "what have you done?" to "who do you know?" It was painful; but no-one was going to errect a statue to me for sticking to the "right values", and if they did, then probably the epitaph would read something like; Despite superhuman efforts, Rob Mellor died in poverty, bitter after enduring enormous privation to reach a better understanding of root nodules. You've gotta be joking!|
Thus I found biology in Denmark to be flogging a dead horse (with the notable exceptions of David Collinge and Shakuntala Thilsted), but fortunately I also realized there was plenty of money to be made in computing and Internet, techniques I could quickly master due to my first degree (computing and biology). I practiced by programming several web-sites, but had already realized that the real problem with Internet was not how to program it, but how to use it and especially how to reorganise the business processes in organisations to take it into account. Thus I put my company into voluntary liquidation and started a 2-year major project "Internet-izing" a travel agent in Copenhagen, raising the bureau to Scandinavias largest.
By now I was quite a "guru" in Internet, BPR and marketing, but several of my theories were mere opinions, not backed up by rigorous research. So I returned to academia, lecturing at the newly formed "IT-University of Copenhagen" in Innovation, Internet Marketing and, later, in E-Learning. Fortunately by books and courses were well received, and even won a couple of prizes. My research was in 3 areas:
1. In Innovationone normally discerns between "invention innovation" and "creativity innovation". I postulated a third type, "diversity innovation". However different types of specialists talking to each other takes a lot of time, and often initially results in chaos because they have difficulty understanding each others mental concepts. I could prove that multi-skilled (or "multi-specialized") people have a much greater chance of being "innovation nuclei" because of the lower transaction costs for communication. My trans-national studies also showed that foreigners (called CED’s, people culturally and/or ethnically different from the people in the SME’s home nation) were especially prominent amongst innovation nuclei, because this group has been exposed to especially high retraining pressures, but that CED’s in companies working in mature markets (as opposed those within immature markets), experienced difficulty in spreading innovations within their environment, possibly because of their large distance from the leadership/consensus group, as defined by A-I Theory. Indeed, in mature markets, innovations by CED’s provoked a Trickle Down effect, which could result in serious consequences for both employer and employee. I postulated the business creation is powered by "invention innovation" and "creativity innovation", but that "diversity innovation" powers business growth.
2. Research inInternet Marketing showed that many generally assumed concepts are misleading:
3. Research ine-learning showed that exposing groups of students to e-learning modules during their course led to a lower average score than amongst control groups (those on the same course without exposure to the e-learning module). Closer analysis revealed:
Thus I showed that adding e-learning modules to classroom teaching does not help improve scores, but it does encourage the weak students not to drop out, but to remain and participate in the exam (where their scores may help lower the class average).
Why so few publications today?
Sometimes people ask me why I publish so few research articles now. The answer is twofold:
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