Re: [ccp4bb] AW: [EXTERNAL] Re: [ccp4bb] AW: [ccp4bb] challenges in structural biology
Dear Patrick, plants do have a rather complex immune system. best regards, Michael On September 21, 2019 10:18:39 AM GMT+02:00, Patrick Shaw Stewart wrote: >Dear Herman > >Animals that are sick tend not to move around a lot. One can imagine >that >this limits the tendency for animal viruses and other animal pathogens >to >become more and more virulent, because the very virulent strains won't >spread as fast. And (importantly) when the most virulent strains >finally >arrive at some particular location, they will find that their potential >hosts are already immune*. > >Since plants don't move around, I have always wondered why plant >pathogens >don't increase in virulence until they wipe out their hosts, especially >when you bear in mind that plants don't have complex immune systems. > >Could these multiple genes be a way to avoid being wiped out by >disease? >Ie if the plant gets sick, it just switches on a batch of "reserve" >genes**. Is that possible? > >Thx, Patrick > > >* This is a pet theory of mine: https://oldwivesandvirologists.blog > >**Or maybe the expression of these genes is random - two genetically >identical individuals growing side-by-side might express different >batches >of genes on a random basis. Again, this might be mainly about disease >prevention. > > > >On Fri, Sep 20, 2019 at 8:51 AM wrote: > >> Dear John, >> >> Plants cannot walk away to a more favorable spot. They remain stuck >where >> they germinate, e.g. whether the place is sunny, shady, wet, dry, >fertile, >> poor etc. So plants compensate by having a lot of genes available to >be >> able to adapt to the particular spot where happen to be. And indeed, >plants >> have usually more genes then animals! >> >> Best, >> >> Herman >> >> >> >> *Von:* CCP4 bulletin board [mailto:CCP4BB@JISCMAIL.AC.UK] *Im Auftrag >von >> *John R Helliwell >> *Gesendet:* Freitag, 20. September 2019 09:19 >> *An:* CCP4BB@JISCMAIL.AC.UK >> *Betreff:* [EXTERNAL] Re: [ccp4bb] AW: [ccp4bb] challenges in >structural >> biology >> >> >> >> *EXTERNAL : *Real sender is owner-ccp...@jiscmail.ac.uk >> >> >> >> Dear Martin, >> >> Many thanks for these details of the size of the human genome over >the >> decades and also the news of your most interesting upcoming review. I >shall >> read it with great interest. >> >> Incidentally is the over 4 genes for the rice genome number >correct? >> This number caught my eye as being interesting how the rice genome is >more >> complicated than our genome. >> >> Best wishes, >> >> John >> >> Emeritus Professor John R Helliwell DSc >> >> >> >> >> >> >> >> >> On 19 Sep 2019, at 08:35, Kollmar, Martin >wrote: >> >> Dear John, >> >> the „100,000 human genes“ is a long-standing myth broad forward by >the >> initiators of the U.S. human genome sequencing projects in 1990. This >large >> number completely contradicted all genetics and mutation data since >the 1940 >> th, but the sequencing community (genome, cDNA, EST) didn’t read even >the >> standard text books. Thus, the “30,000” genes published with the two >human >> genome papers in 2001 are not “surprisingly low” but just in >accordance >> with the predictions and the data since the 1940th. The gene number >went >> down to about 23,000 already in 2004, and the current numbers >(depending on >> database) range around 20,000 human protein-coding genes. The myth of >the >> large numbers is only propagated by those who profit from larger >numbers >> (e.g. bigger grants, papers in higher IF journals, big consortia). >> >> >> >> I have written a review about the current state (and history) of the >human >> protein-coding genes, which will appear online in BioEssays soon and >> finally in the November issue (will be open access). In this review >there >> will be some (hopefully) useful plots showing the gene numbers since >the >> 1940th and a detailed review of all the numbers and their >experimental >> basis (most were actually just extrapolations from small-scale data). >> >> >> >> Please excuse this kind of self-advertisement, but it is really more >than >> time to move this myth out of science literature and communication. >> >> >> >> Best regards, >> >> Martin >> >> >> >> Priv. Doz. Dr. Martin Kollmar >> >> >> >> Group S
Re: [ccp4bb] AW: [EXTERNAL] Re: [ccp4bb] AW: [ccp4bb] challenges in structural biology
Dear Herman Animals that are sick tend not to move around a lot. One can imagine that this limits the tendency for animal viruses and other animal pathogens to become more and more virulent, because the very virulent strains won't spread as fast. And (importantly) when the most virulent strains finally arrive at some particular location, they will find that their potential hosts are already immune*. Since plants don't move around, I have always wondered why plant pathogens don't increase in virulence until they wipe out their hosts, especially when you bear in mind that plants don't have complex immune systems. Could these multiple genes be a way to avoid being wiped out by disease? Ie if the plant gets sick, it just switches on a batch of "reserve" genes**. Is that possible? Thx, Patrick * This is a pet theory of mine: https://oldwivesandvirologists.blog **Or maybe the expression of these genes is random - two genetically identical individuals growing side-by-side might express different batches of genes on a random basis. Again, this might be mainly about disease prevention. On Fri, Sep 20, 2019 at 8:51 AM wrote: > Dear John, > > Plants cannot walk away to a more favorable spot. They remain stuck where > they germinate, e.g. whether the place is sunny, shady, wet, dry, fertile, > poor etc. So plants compensate by having a lot of genes available to be > able to adapt to the particular spot where happen to be. And indeed, plants > have usually more genes then animals! > > Best, > > Herman > > > > *Von:* CCP4 bulletin board [mailto:CCP4BB@JISCMAIL.AC.UK] *Im Auftrag von > *John R Helliwell > *Gesendet:* Freitag, 20. September 2019 09:19 > *An:* CCP4BB@JISCMAIL.AC.UK > *Betreff:* [EXTERNAL] Re: [ccp4bb] AW: [ccp4bb] challenges in structural > biology > > > > *EXTERNAL : *Real sender is owner-ccp...@jiscmail.ac.uk > > > > Dear Martin, > > Many thanks for these details of the size of the human genome over the > decades and also the news of your most interesting upcoming review. I shall > read it with great interest. > > Incidentally is the over 4 genes for the rice genome number correct? > This number caught my eye as being interesting how the rice genome is more > complicated than our genome. > > Best wishes, > > John > > Emeritus Professor John R Helliwell DSc > > > > > > > > > On 19 Sep 2019, at 08:35, Kollmar, Martin wrote: > > Dear John, > > the „100,000 human genes“ is a long-standing myth broad forward by the > initiators of the U.S. human genome sequencing projects in 1990. This large > number completely contradicted all genetics and mutation data since the 1940 > th, but the sequencing community (genome, cDNA, EST) didn’t read even the > standard text books. Thus, the “30,000” genes published with the two human > genome papers in 2001 are not “surprisingly low” but just in accordance > with the predictions and the data since the 1940th. The gene number went > down to about 23,000 already in 2004, and the current numbers (depending on > database) range around 20,000 human protein-coding genes. The myth of the > large numbers is only propagated by those who profit from larger numbers > (e.g. bigger grants, papers in higher IF journals, big consortia). > > > > I have written a review about the current state (and history) of the human > protein-coding genes, which will appear online in BioEssays soon and > finally in the November issue (will be open access). In this review there > will be some (hopefully) useful plots showing the gene numbers since the > 1940th and a detailed review of all the numbers and their experimental > basis (most were actually just extrapolations from small-scale data). > > > > Please excuse this kind of self-advertisement, but it is really more than > time to move this myth out of science literature and communication. > > > > Best regards, > > Martin > > > > Priv. Doz. Dr. Martin Kollmar > > > > Group Systems Biology of Motor Proteins > > Department NMR-based Structural Biology > > Max-Planck-Institute for Biophysical Chemistry > > Am Fassberg 11 > > 37077 Goettingen > > Deutschland > > > > www.motorprotein.de > <https://urldefense.proofpoint.com/v2/url?u=http-3A__www.motorprotein.de_=DwMFaQ=Dbf9zoswcQ-CRvvI7VX5j3HvibIuT3ZiarcKl5qtMPo=HK-CY_tL8CLLA93vdywyu3qI70R4H8oHzZyRHMQu1AQ=32JRE8HZHPdJxpaoz1sLz-PnTi-D_zZTMfdQs_FdEcI=IWuNyBzheAGJ761iddc78L4lz7sB21cKQTrawbV4j0M=> > (Homepage) > > www.cymobase.org > <https://urldefense.proofpoint.com/v2/url?u=http-3A__www.cymobase.org_=DwMFaQ=Dbf9zoswcQ-CRvvI7VX5j3HvibIuT3ZiarcKl5qtMPo=HK-CY_tL8CLLA93vdywyu3qI70R4H8oHzZyRHMQu1AQ=32JRE8HZHPdJxpaoz1sLz-P
