Cell Trends
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Cell Nucleus Surface More Complicated than Expected 06/14/2001
Researchers at North Carolina State University made an unexpected discovery: cell nuclear membranes are groovy. The surfaces of some plant cells were found to contain tunnels and grooves with complex channels used by RNA, enzymes and organelles to enter and exit the cell’s master control center. They found that parts of the endoplasmic reticulum (a system of folded channels) passes right into the center of the nucleus, and watched organelles moving along actin filaments in the grooves. Dr. Nina Allen, botanist at the university, said, “The implication of this discovery is that we need to look more closely at communications between the nucleus and the cytoplasm, and we need to understand why these grooves and tunnels are there.”
What they witnessed was a highly complex transportation system at work. Imagine a city with overlapping monorails shuttling cargo loads in all directions, with loading docks, signalling systems and security checks: this is what goes on in miniature inside the cell. The picture of the cell that is being slowly revealed to our instruments is one of bewildering complexity. Every day, it becomes increasingly difficult to imagine Darwinism surviving the onslaught of such discoveries.
Researchers at North Carolina State University made an unexpected discovery: cell nuclear membranes are groovy. The surfaces of some plant cells were found to contain tunnels and grooves with complex channels used by RNA, enzymes and organelles to enter and exit the cell’s master control center. They found that parts of the endoplasmic reticulum (a system of folded channels) passes right into the center of the nucleus, and watched organelles moving along actin filaments in the grooves. Dr. Nina Allen, botanist at the university, said, “The implication of this discovery is that we need to look more closely at communications between the nucleus and the cytoplasm, and we need to understand why these grooves and tunnels are there.”
What they witnessed was a highly complex transportation system at work. Imagine a city with overlapping monorails shuttling cargo loads in all directions, with loading docks, signalling systems and security checks: this is what goes on in miniature inside the cell. The picture of the cell that is being slowly revealed to our instruments is one of bewildering complexity. Every day, it becomes increasingly difficult to imagine Darwinism surviving the onslaught of such discoveries.
gimme some numbers .. any numbers ... anything you think might be reasonable ..
im guessing you think 4 billion years is reasonable for the age of life on earth...
im guessing that mutations propogated by natural selection should be less than 1 per 100 years ..
what does that put the total mutations propogated at?
this is among the simplest of maths equations .. division .. and youre dodging it like its complex differentiation.
im guessing you think 4 billion years is reasonable for the age of life on earth...
im guessing that mutations propogated by natural selection should be less than 1 per 100 years ..
what does that put the total mutations propogated at?
this is among the simplest of maths equations .. division .. and youre dodging it like its complex differentiation.
you disagree with everything i say and claim reason is all on your side ... i do much the same ... so its likely that discussions between the two of us will quickly degenerate.
care to explain why we are so the same yet diametrically opposed?
care to explain why we are so the same yet diametrically opposed?
See, when you start making up numbers and "guessing" you can't possibly come to the right conclusion. It doesn't help anybody. We might as well make up numbers and claim they tell our future. The number of deleterious mutations integrated into the human genome has been estimated at 4 per generation. There are a number of studies assessing the number of mutations that must have occured since we diverged from apes. You might want to look into those studies which are more specific and measured more accurately instead of trying to make up the average number of mutations for all the species on the planet over the past 4 billion years.Stipe said:
The problem is that "mutations per year" tells us nothing. In what organism? Bacteria undoubtedly have much higher populational rates simply because more individuals exist and reproduce per hundred years. On the other hand, larger genomes are more likely to aquire a mutation simply based on probability.
holy sorry crap. ITS LONG DIVISION FOR GOODNESS SNAKES!
it doesnt MATTER what random numbers i plug in there ...
4 billion divided by 10^40000 equals ..?
14 billion divided by 10^40001 equals..?
4 billion divided by 1 equals..?
4 divided by 4 billion equals..?
8046 divided by 0 equals..?
4 billion divided by infinity equals..?
4 billion divided by your brain equals..?
what matters is that its LONG DIVISION .. and you should not be afraid of plugging numbers youre comfortable with into a simple maths equation..
you are scared and are DESPERATELY searching for a way not to do so .. because you know youll get laughed at no matter what fictional numbers you come up with.
it doesnt MATTER what random numbers i plug in there ...
4 billion divided by 10^40000 equals ..?
14 billion divided by 10^40001 equals..?
4 billion divided by 1 equals..?
4 divided by 4 billion equals..?
8046 divided by 0 equals..?
4 billion divided by infinity equals..?
4 billion divided by your brain equals..?
what matters is that its LONG DIVISION .. and you should not be afraid of plugging numbers youre comfortable with into a simple maths equation..
you are scared and are DESPERATELY searching for a way not to do so .. because you know youll get laughed at no matter what fictional numbers you come up with.
Plants Talk to Themselves in Email 07/13/2001
How does one part of a plant know that another part is under attack, or how do the roots know the weather is changing and affecting the leaves? According to Nature, plants have a busy system of email messages spreading the news. Scientists have discovered messenger RNA (mRNA) molecules travelling from cell to cell and onto their own little Internet (the phloem), that apparently let one part of the plant know what’s going on in another part.
Look at the nearest plant and stare at it for awhile. It seems so static and motionless; did you have any idea this beehive of communication was going on? Now look at a rock for comparison. Evolutionists have to get from one to the other; it’s like believing a desolate planet, pockmarked with craters and exposed to deadly radiation, somehow spontaneously developed its own Internet.
How does one part of a plant know that another part is under attack, or how do the roots know the weather is changing and affecting the leaves? According to Nature, plants have a busy system of email messages spreading the news. Scientists have discovered messenger RNA (mRNA) molecules travelling from cell to cell and onto their own little Internet (the phloem), that apparently let one part of the plant know what’s going on in another part.
Look at the nearest plant and stare at it for awhile. It seems so static and motionless; did you have any idea this beehive of communication was going on? Now look at a rock for comparison. Evolutionists have to get from one to the other; it’s like believing a desolate planet, pockmarked with craters and exposed to deadly radiation, somehow spontaneously developed its own Internet.
aharvey
New member
The last phrase (starting with ".. because") is technically true given that you guys laugh at facts and at logic we present, so why would we expect any different with hypothetical data?stipe said:
Just for yuks, here are a few relevant numbers for you: roughly one mutation occurs per one million gene replications, of which 1/1,000,000 might be beneficial and thus stand a decent chance, let's say p, at getting incorporated into the genome of the species). The product of those numbers (1/1,000,000 * 1/1,000,000 * p) is pretty darn small alright! But now multiply that product by the number of genes in an organism times the number of gametes each organism is likely to produce during one reproductive season (mutations occur in somatic cells but this is not terribly relevant for evolutionary questions) times the number of reproductive seasons in an individual's lifetime times the number of individuals in the population times the number of reproductive seasons that species has been in existence. That will give you an estimate how many beneficial mutations are likely to have been fixed in the history of that single species. Do that for every species that has ever lived; sum together for a grand total. Then you'll have your answer! And before you complain how this is both impossibly complex and ridiculously ovesimplified, remember how you asked us to approach it!
And don't forget that a huge fraction of these changes are cumulative, inherited. We don't need 10 million separate evolutionary events to account for the fact that 10 million species of insects have three pairs of legs.
aharvey
New member
I gave you the way to think about the problem. Let's try something different that will hopefully illustrate better why your fixation on mutations per year is misplaced.stipe said:
Start with one bacteria, of a sluggish species whose population size only doubles each day.
Day 1: one bacteria; day 2: two bacteria, day 3: four bacteria, day 4: eight bacteria, etc.
Just like in mutations, the number of bacterial births depends on both the per capita rate and the population size. So what does the average tell us? After 4 days, we have seven new bacteria, for an average of 1.75 new bacteria per day. After 10 days, we'd have 1023 new bacteria, for an average of 102.3 new bacteria per day. After 40 days, we'd have 1.09951E+12 new bacteria, for an average of 27,487,790,694 new bacteria per day. So what does the average tell us?
Alright Stipe, I'll play your game with data that we have available.
Assumptions:
1) Bacterial genome at 4 million base pairs, replicating every 17 minute, one mutation per 300 chromosome replications. Our e.coli has a population density of about 3x10^8 cells/mL [All of these are empirical measurements you can look up if you doubt me]
2) Four billion years of replication
At one replication every 17 minutes, that's 122640000000000 replications in 4 billion years for A SINGLE LINE.
BUT, recall that each replication actually produces 2 bacteria and thus the colony grows exponentially. So for the sake of absurd conservatism, lets say the population stops exponentially expanding after 35 replications but still replicates at this steady-state populational level. That means our population of e.coli is now 34359738368 cells. (To help you understand how underestimated this count is, this number of e.coli cells at the density above is about 1/2 cup. In four billion years, this 1/2 cup of cells would have 4213878313451520000000000 replications (assuming adequate food supply). That leaves us with 14046261044838400000000 MUTATIONS occuring, and if only 1/1,000,000 are beneficial that's 14046261044838400 BENEFICIAL MUTATIONS, more than enough to account for the e.coli's current genome.
Shall we play again with different numbers?
Edit: I see aharvey beat me to the punch.
Edit #2: Fixed values.
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Clones Express Genes Differently 07/06/2001
Why do so many cloned embryos die before birth? Why do the ones that survive have abnormalities? According to scientists at MIT reported by Scientific American News, it’s because clones express genes differently than the donor; i.e., even though the donor and the clone have identical DNA, they do not activate the same genes in the same way. Apparently there are “epigenetic” factors at work, influences other than the coded language of life. These include enzyme tags on genes that affect their expression. Embryonic stem cells with nuclei from donors can have different tags that cause them to develop in wildly different ways, producing chimeras (monsters), abnormally large offspring, or survivors that while appearing outwardly normal have hidden abnormalities that can lead to problems later.
The statement that the DNA is the master molecule that accounts for everything in life may be too simplistic. What are all the epigenetic factors that influence development? Are any of them heritable? How do cells know which genes to express in which part of the body, even though the entire code is present? We don’t know, but the science of cloning is showing just how complex a process development is, and the ramifications have ethical and political overtones.
Why do so many cloned embryos die before birth? Why do the ones that survive have abnormalities? According to scientists at MIT reported by Scientific American News, it’s because clones express genes differently than the donor; i.e., even though the donor and the clone have identical DNA, they do not activate the same genes in the same way. Apparently there are “epigenetic” factors at work, influences other than the coded language of life. These include enzyme tags on genes that affect their expression. Embryonic stem cells with nuclei from donors can have different tags that cause them to develop in wildly different ways, producing chimeras (monsters), abnormally large offspring, or survivors that while appearing outwardly normal have hidden abnormalities that can lead to problems later.
The statement that the DNA is the master molecule that accounts for everything in life may be too simplistic. What are all the epigenetic factors that influence development? Are any of them heritable? How do cells know which genes to express in which part of the body, even though the entire code is present? We don’t know, but the science of cloning is showing just how complex a process development is, and the ramifications have ethical and political overtones.
Human Genome 07/10/2001: The BBC reports that some scientists dispute earlier estimates that the human genome only has 30,000 genes. Using different statistical techniques, they claim it has over twice as many: 70,000 or more.
Update 08/24/2001: A report in Nature puts the number at 42,000 but admits it could go higher than 50,000. One of the difficulties is the algorithms used to estimate the number of genes, and the lack of knowledge of function of various sequences. (Earlier reference: February 2001 headline).
Update 11/28/2001: According to EurekAlert, scientists at Cold Spring Harbor laboratories, Long Island NY, now have a computer program able to spot gene "on" switches and promoters. They think the number of human genes is now between 50,000 and 60,000.
See also the report in the Feb 22, 2002 issue of Science about discussion among members of the AAAS.
Update 08/24/2001: A report in Nature puts the number at 42,000 but admits it could go higher than 50,000. One of the difficulties is the algorithms used to estimate the number of genes, and the lack of knowledge of function of various sequences. (Earlier reference: February 2001 headline).
Update 11/28/2001: According to EurekAlert, scientists at Cold Spring Harbor laboratories, Long Island NY, now have a computer program able to spot gene "on" switches and promoters. They think the number of human genes is now between 50,000 and 60,000.
See also the report in the Feb 22, 2002 issue of Science about discussion among members of the AAAS.
25 Years of Study on DNA Copy and Repair Mechanisms Summarized 07/18/2001
The July 17 issue of the Proceedings of the National Academy of Sciences contains a long paper by two MIT biochemists on what we have learned so far in 25 years of study of enzymes that help copy and repair DNA: the DNA polymerases. Apparently these wonder molecules not only synthesize DNA but repair a number of different kinds of errors. The coordination of which polymerase is activated and tosses the baton to another is still poorly understood. Most of the work has been done on E. coli, a prokaryote (simpler one-celled organisms lacking a nucleus), but the situation is even more complex in the eukaryotes (all higher organisms), “where both the number of DNA polymerases and the level of complexity of the events are far greater.”
If your brain can tolerate the technical jargon without crashing, and if you need evidence for a Designer, you should read this paper. The authors seem truly amazed at the performance of these submicroscopic molecules. Some sample sentences:
• A common, defining feature of these DNA polymerases is a remarkable ability to replicate imperfect DNA templates . . .
• The recent discovery of additional eukaryotic DNA polymerases...further complicates the already daunting issue of understanding the control systems that govern which DNA polymerase gains access . . . .
• A growing body of evidence suggests that an important additional level of control results from DNA polymerases being "coached" as to their correct biological role through interactions with other proteins associated with the particular DNA substrate . . . .
• In addition to their roles in chromosomal DNA replication, DNA polymerases participate in numerous DNA repair pathways, including double-strand break repair, mismatch repair, base excision repair and nucleotide excision repair . . . .
• Elaborate regulatory controls and a sophisticated system of protein-protein contacts ensure that the...gene products carry out their appropriate biological roles. However, as is so often the case in science, the discoveries of today are posing even more challenging questions for tomorrow.
And this all takes place in the simplest kinds of bacteria! Remember that Darwin did not know any of this. To the Darwinians, cells were little blobs of unknown stuff called “protoplasm” and it was easy to talk glibly about it arising in some warm little pond and evolving into higher organisms. As Michael Behe said, the cell was a “black box” to Darwin, but now we have opened the box and are staring with awe at the contents. Does a system as complex as a robotic factory, complete with fail-safe mechanisms, feedback, automatic repair and inspectors originate out of ooze? No way! Darwin himself said, “If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find no such case.” Well, biochemistry is providing cases by the truckload. How do you spell DNA? “Darwinism Not Adequate.”
The July 17 issue of the Proceedings of the National Academy of Sciences contains a long paper by two MIT biochemists on what we have learned so far in 25 years of study of enzymes that help copy and repair DNA: the DNA polymerases. Apparently these wonder molecules not only synthesize DNA but repair a number of different kinds of errors. The coordination of which polymerase is activated and tosses the baton to another is still poorly understood. Most of the work has been done on E. coli, a prokaryote (simpler one-celled organisms lacking a nucleus), but the situation is even more complex in the eukaryotes (all higher organisms), “where both the number of DNA polymerases and the level of complexity of the events are far greater.”
If your brain can tolerate the technical jargon without crashing, and if you need evidence for a Designer, you should read this paper. The authors seem truly amazed at the performance of these submicroscopic molecules. Some sample sentences:
• A common, defining feature of these DNA polymerases is a remarkable ability to replicate imperfect DNA templates . . .
• The recent discovery of additional eukaryotic DNA polymerases...further complicates the already daunting issue of understanding the control systems that govern which DNA polymerase gains access . . . .
• A growing body of evidence suggests that an important additional level of control results from DNA polymerases being "coached" as to their correct biological role through interactions with other proteins associated with the particular DNA substrate . . . .
• In addition to their roles in chromosomal DNA replication, DNA polymerases participate in numerous DNA repair pathways, including double-strand break repair, mismatch repair, base excision repair and nucleotide excision repair . . . .
• Elaborate regulatory controls and a sophisticated system of protein-protein contacts ensure that the...gene products carry out their appropriate biological roles. However, as is so often the case in science, the discoveries of today are posing even more challenging questions for tomorrow.
And this all takes place in the simplest kinds of bacteria! Remember that Darwin did not know any of this. To the Darwinians, cells were little blobs of unknown stuff called “protoplasm” and it was easy to talk glibly about it arising in some warm little pond and evolving into higher organisms. As Michael Behe said, the cell was a “black box” to Darwin, but now we have opened the box and are staring with awe at the contents. Does a system as complex as a robotic factory, complete with fail-safe mechanisms, feedback, automatic repair and inspectors originate out of ooze? No way! Darwin himself said, “If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find no such case.” Well, biochemistry is providing cases by the truckload. How do you spell DNA? “Darwinism Not Adequate.”