Information

Do changes in an organism's cell modify the genetic information it uses for reproduction?


What I'm actually interested about is whether a modification in one cell during the life of an asexually reproducing organism affects its genetic information? Which cell's genetic information is used during reproduction like budding, for example in the case of Hydra.

Or does the incidental advantage it could have given rise to disappear with the death of the organism?


In multicellular organisms there are specialised cells called gametes that are responsible for sexual reproduction (sperm/ egg cells). Mutations occurring in these cells can be passed on to offspring (germ line mutations). Mutations occurring in others cells affect only the given individual (somatic mutations).

Edit: For unicellular organisms it is pretty straight forward, the daughter cells formed through fission are identical. As for multicellular organisms here are many forms of asexual reproduction, and even these may involve the formation of specialized cells (eg. spores). So my answer is: it depends on the type of asexual reproduction and the actual cell(s) that accumulate mutation(s). For example in parthenogenesis - where the unfertilized egg cell develops into a new individual - , a mutation can be inherited if it occurs in the germ line cells generating the egg cell, but any somatic mutation would stay in the parent. You can find detailed info on asexual reproduction with details on each form on this wiki page


Would something like CRISPR fit your criteria? CRISPR is essentially an adaptive immune system for bacteria. When a bacteria encounters foreign DNA (usually from an invading bacteriophage), it can cut it up and insert part of it in between palindromic repeats called CRISPRs. This small piece of DNA can be transcribed and then used as a template to recognize other copies of the foreign DNA. When a match is found, the foreign DNA is degraded, impairing the invading virus. Because a record of this foreign DNA is stored in the bacterial chromosome, it is transmitted to daughter cells, which will now have some protection against the offending virus in the future.

In the same vein, when certain bacteriophages invade bacteria, they integrate their viral genomes into the host bacterial genome---phage lambda is the classic example. At this juncture, the phage can choose between two lifestyles: lysis, in which the virus replicates like crazy, killing the host cell and spreading to other cells; or lysogeny, in which the virus lies dormant, allowing its genome to hitch a ride in the host genome, getting replicated and passed on to daughter cells just like any other piece of chromosomal DNA. When the time is right, the virus can switch back to lysis, proliferate, and infect new cells. Thus viral invasion of an asexually reproducing organism can lead to heritable changes in the host genome.

I'm sure you've heard of epigenetics, in which environmental factors can cause heritable changes to an organism without specifically mutating genes. While typically appreciated in eukaryotic organisms, asexually reproducing bacteria also have epigenetic mechanisms (1).

(1): Casadesus J and Low D. (2006). Epigenetic gene regulation in the bacterial world. Microbiol. Mol. Biol. Rev. 70(3): 830-56.


Scientists Change Biology with Technology

Imagine storing digital information in deoxyribonucleic acid (DNA), the substance that carries genetic information in the cells of living things.

What about wearing a device that makes you more intelligent or creating new materials by changing the genes of microorganisms?

These ideas may sound unreal, but scientists are creating technologies that use their knowledge of biology and make changes with a computer. These scientists are working with artificial intelligence (AI), using the power of computers to copy intelligent human behavior.

Some of the researchers presented their findings at the 2018 Milken Institute Global Conference. The meeting was held recently in Los Angeles, California.

The researchers spoke at a group discussion called “Things That Will Blow Your Mind.”

“The machine finds stuff in biology that a human would never find,” said Joshua Hoffman, chief executive officer of Zymergen. He said his company is performing experiments that would never have been possible just a few years ago.

Changing microbial genes

Zymergen uses computers to design experiments that change the genetic structure of microorganisms. As a result of the changes, the chemicals produced by microbes can make stronger or better materials.

“We use automation and machine learning to engineer microbes… to turn them into the chemical factories of the future,” Hoffman said. “What we’re doing is we’re searching the genome for the things that might work. What machine learning does is it looks for patterns that a human wouldn’t find in ways that are more likely than not to have the genetic changes in the genome that are going to have the impact, the trait, that we want.”

Hoffman said that what takes humans years to discover, computers can do in months. His company works mainly with the chemicals and materials industry, as well as agricultural companies.

He added that Zymergen works on creating non-harmful chemical products that protect plants from disease.

Improving the human brain

Vivienne Ming set up Socos Labs, an independent research group.

Ming studies how the brain works. She wants to know if it is possible to make human beings more intelligent by physically putting things into their brain.

“How much you can think about, pay attention to, mentally operate on at any given moment . we’ve actually found that we can increase that by about 15 percent,” she said.

Laboratories around the world are already studying different ways to improve the brain’s cognition and treat conditions like autism and depression.

Ming said one example of how this research could help is by improving the cognition of under-served children.

Instead of requiring students to attend special classes, Ming said, “We might actually be able to use that technology that brings them right back up with the rest of the kids.”

In a world with artificial intelligence, improving cognition is one way for humans to compete with machines, she added.

DNA information storage

Hyunjun Park and his company, Catalog, make artificial DNA used to store digital information.

Park warned that since people are creating so much information from the internet, social media, and wireless communications, we soon will not have enough space to store it. He feels we need a new way to save this information.

Park said current digital forms of information storage take up lot of land and city space. It also costs lots of money to supervise.

However, Park feels that DNA can store much more information, and that it can last thousands of years. He says his company has learned how to do it for less money than other laboratories.

Park said his company’s researchers use a liquid, which they move to look like different pieces of DNA. Then, for storage, they dry it into particles, which are stored in a container.

He said an industrial size model for DNA storage can be ready as early as 2019.

Park says that as biology scientists continue to explore the future of artificial intelligence, investors are starting to pay attention.

“These traditional investors…they are now looking at biotech and seeing this as really the future of innovation,” Park said.

Elizabeth Lee reported this story for VOANews.com. Phil Dierking adapted her report for Learning English. George Grow was the editor.

What do you think they will learn about Mars? Write to us in the Comments Section or on our Facebook page.


How an Asexual Lizard Procreates Alone

All moms and no dads, the whiptail still comes up with genetically diverse offspring.

N. Mexico Whiptail Lizard

Without females, lizards in the Aspidoscelis genus, like this New Mexico Whiptail (Aspidoscelis neomexicana), reproduce asexually. Unlike other animals that produce this way, however, their DNA changes from generation to generation.

Photograph by Bill Gorum/Alamy Stock Photo

In sexual reproduction&mdashthe way most life-forms procreate&mdasheach parent provides half an offspring's chromosomes. Over generations, this mating and procreating shuffles the DNA deck, giving sexual reproducers a genetic diversity that helps them adapt to changing environments.

By contrast, asexual reproducers&mdashsome 70 vertebrate species and many less-complex organisms&mdash"use all the chromosomes they have" to solitarily produce offspring that are genetic clones, molecular biologist Peter Baumann says. Because the organisms are genetically identical, they're more vulnerable: A disease or an environmental shift that kills one could kill all.

But there's a twist in the case of the genus Aspidoscelis, the asexually reproducing whiptail lizards that Baumann and his colleagues have been studying at the United States' Stowers Institute for Medical Research in Kansas City, Missouri. The lizards are all female and parthenogenetic, meaning their eggs develop into embryos without fertilization.

But before the eggs form, Baumann's team discovered, the females' cells gain twice the usual number of chromosomes during meiosis. This results in a standard pair of chromosones derived from two sets of pairs. So the eggs get a full chromosome count and genetic variety and breadth (known as heterozygosity) rivaling that of a sexually reproducing lizard.

Why does this occur? Because long ago, Baumann says, lizards of the genus Aspidoscelis had "a hybridization event"&mdashthat is, females of one species broke form and mated with males of another species. Those outlier liaisons gave whiptails robust heterozygosity, which has been preserved by the identical replication&mdashessentially, cloning&mdashthat occurs in asexual reproduction. It's a genetic-diversity advantage that today's females still enjoy and propagate.

Without females, lizards in the Aspidoscelis genus, like this New Mexico Whiptail (Aspidoscelis neomexicana), reproduce asexually. Unlike other animals that produce this way, however, their DNA changes from generation to generation.


Genetic Engineering 2.0: An On-Off Switch for Gene Editing

A new CRISPR method allows researchers to silence most genes in the human genome without altering the underlying DNA sequence — and then reverse the changes. Credit: Jennifer Cook-Chrysos/Whitehead Institute

New, reversible CRISPR method can control gene expression while leaving underlying DNA sequence unchanged.

Over the past decade, the CRISPR-Cas9 gene editing system has revolutionized genetic engineering, allowing scientists to make targeted changes to organisms’ DNA. While the system could potentially be useful in treating a variety of diseases, CRISPR-Cas9 editing involves cutting DNA strands, leading to permanent changes to the cell’s genetic material.

Now, in a paper published online in Cell on April 9, researchers describe a new gene editing technology called CRISPRoff that allows researchers to control gene expression with high specificity while leaving the sequence of the DNA unchanged. Designed by Whitehead Institute Member Jonathan Weissman, University of California San Francisco assistant professor Luke Gilbert, Weissman lab postdoc James Nuñez and collaborators, the method is stable enough to be inherited through hundreds of cell divisions, and is also fully reversible.

“The big story here is we now have a simple tool that can silence the vast majority of genes,” says Weissman, who is also a professor of biology at MIT and an investigator with the Howard Hughes Medical Institute. “We can do this for multiple genes at the same time without any DNA damage, with great deal of homogeneity, and in a way that can be reversed. It’s a great tool for controlling gene expression.”

The project was partially funded by a 2017 grant from the Defense Advanced Research Projects Agency to create a reversible gene editor. “Fast forward four years [from the initial grant], and CRISPRoff finally works as envisioned in a science fiction way,” says co-senior author Gilbert. “It’s exciting to see it work so well in practice.”

Genetic engineering 2.0

The classic CRISPR-Cas9 system uses a DNA-cutting protein called Cas9 found in bacterial immune systems. The system can be targeted to specific genes in human cells using a single guide RNA, where the Cas9 proteins create tiny breaks in the DNA strand. Then the cell’s existing repair machinery patches up the holes.

Because these methods alter the underlying DNA sequence, they are permanent. Plus, their reliance on “in-house” cellular repair mechanisms means it is hard to limit the outcome to a single desired change. “As beautiful as CRISPR-Cas9 is, it hands off the repair to natural cellular processes, which are complex and multifaceted,” Weissman says. “It’s very hard to control the outcomes.”

That’s where the researchers saw an opportunity for a different kind of gene editor — one that didn’t alter the DNA sequences themselves, but changed the way they were read in the cell.

This sort of modification is what scientists call “epigenetic” — genes may be silenced or activated based on chemical changes to the DNA strand. Problems with a cell’s epigenetics are responsible for many human diseases such as Fragile X syndrome and various cancers, and can be passed down through generations.

Epigenetic gene silencing often works through methylation — the addition of chemical tags to to certain places in the DNA strand — which causes the DNA to become inaccessible to RNA polymerase, the enzyme which reads the genetic information in the DNA sequence into messenger RNA transcripts, which can ultimately be the blueprints for proteins.

Weissman and collaborators had previously created two other epigenetic editors called CRISPRi and CRISPRa — but both of these came with a caveat. In order for them to work in cells, the cells had to be continually expressing artificial proteins to maintain the changes.

“With this new CRISPRoff technology, you can [express a protein briefly] to write a program that’s remembered and carried out indefinitely by the cell,” says Gilbert. “It changes the game so now you’re basically writing a change that is passed down through cell divisions — in some ways we can learn to create a version 2.0 of CRISPR-Cas9 that is safer and just as effective, and can do all these other things as well.”

Building the switch

To build an epigenetic editor that could mimic natural DNA methylation, the researchers created a tiny protein machine that, guided by small RNAs, can tack methyl groups onto specific spots on the strand. These methylated genes are then “silenced,” or turned off, hence the name CRISPRoff.

Because the method does not alter the sequence of the DNA strand, the researchers can reverse the silencing effect using enzymes that remove methyl groups, a method they called CRISPRon.

As they tested CRISPRoff in different conditions, the researchers discovered a few interesting features of the new system. For one thing, they could target the method to the vast majority of genes in the human genome — and it worked not just for the genes themselves, but also for other regions of DNA that control gene expression but do not code for proteins. “That was a huge shock even for us, because we thought it was only going to be applicable for a subset of genes,” says first author Nuñez.

Also, surprisingly to the researchers, CRISPRoff was even able to silence genes that did not have large methylated regions called CpG islands, which had previously been thought necessary to any DNA methylation mechanism.

“What was thought before this work was that the 30 percent of genes that do not have a CpG island were not controlled by DNA methylation,” Gilbert says. “But our work clearly shows that you don’t require a CpG island to turn genes off by methylation. That, to me, was a major surprise.”

CRISPRoff in research and therapy

To investigate the potential of CRISPRoff for practical applications, the scientists tested the method in induced pluripotent stem cells. These are cells that can turn into countless cell types in the body depending on the cocktail of molecules they are exposed to, and thus are powerful models for studying the development and function of particular cell types.

The researchers chose a gene to silence in the stem cells, and then induced them to turn into nerve cells called neurons. When they looked for the same gene in the neurons, they discovered that it had remained silenced in 90 percent of the cells, revealing that cells retain a memory of epigenetic modifications made by the CRISPRoff system even as they change cell type.

They also selected one gene to use as an example of how CRISPRoff might be applied to therapeutics: the gene that codes for Tau protein, which is implicated in Alzheimer’s disease. After testing the method in neurons, they were able to show that using CRISPRoff could be used to turn Tau expression down, although not entirely off. “What we showed is that this is a viable strategy for silencing Tau and preventing that protein from being expressed,” Weissman says. “The question is, then, how do you deliver this to an adult? And would it really be enough to impact Alzheimer’s? Those are big open questions, especially the latter.”

Even if CRISPRoff does not lead to Alzheimer’s therapies, there are many other conditions it could potentially be applied to. And while delivery to specific tissues remains a challenge for gene editing technologies such as CRISPRoff, “we showed that you can deliver it transiently as a DNA or as an RNA, the same technology that’s the basis of the Moderna and BioNTech coronavirus vaccine,” Weissman says.

Weissman, Gilbert, and collaborators are enthusiastic about the potential of CRISPRoff for research as well. “Since we now can sort of silence any part of the genome that we want, it’s a great tool for exploring the function of the genome,” Weissman says.

Plus, having a reliable system to alter a cell’s epigenetics could help researchers learn the mechanisms by which epigenetic modifications are passed down through cell divisions. “I think our tool really allows us to begin to study the mechanism of heritability, especially epigenetic heritability, which is a huge question in the biomedical sciences,” Nuñez says.

Reference: “Genome-wide programmable transcriptional memory by CRISPR-based epigenome editing” by James K. Nuñez, Jin Chen, Greg C. Pommier, J. Zachery Cogan, Joseph M. Replogle, Carmen Adriaens, Gokul N. Ramadoss, Quanming Shi, King L. Hung, Avi J. Samelson, Angela N. Pogson, James Y.S. Kim, Amanda Chung, Manuel D. Leonetti, Howard Y. Chang, Martin Kampmann, Bradley E. Bernstein, Volker Hovestadt, Luke A. Gilbert and Jonathan S. Weissman, 9 April 2021, Cell.
DOI: 10.1016/j.cell.2021.03.025

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4 Comments on "Genetic Engineering 2.0: An On-Off Switch for Gene Editing"

This could help conditions like mine (CMT1A) which is caused by a gene over-expression.

Babu G. Ranganathan*
(B.A. Bible/Biology)

HOW DOES DNA TURN A CELL INTO A SHEEP, OR A BIRD, OR A HUMAN?

When you divide a cake, the cake never gets bigger. However, when we were just a single cell and that cell kept dividing we got bigger. New material had to come from somewhere. That new material came from food.

Just as the sequence of various letters and words in human language communicate a message and direct workers to build and assemble something so, too, the sequence of various molecules in our DNA (our genes or genetic code) directed the molecules from our mother’s food, that we received in the womb, to become new cells, eventually forming all the tissues and organs of our body.

When you feed a cat your food the cat’s DNA will direct the food molecules to become the cells, tissues, and organs of a cat, but your DNA will turn the same food into human cells, tissues, and organs.

What we call “genes” are actually segments of the DNA molecule. When you understand how your DNA works, you’ll also understand how egg yolks can turn into chickens. Read my popular Internet article: HOW DID MY DNA MAKE ME? Just google the title to access the article.

This article will give you a good understanding of how DNA, as well as cloning and genetic engineering. You also learn that so-called “Junk DNA” isn’t junk at all. You will learn why it is not rational to believe that DNA code could have arisen by chance. Science points (not proves, but points) to an intelligent cause for DNA code.

What about genetic and biological similarities between species? Genetic information, like other forms of information, cannot happen by chance, so it is more logical to believe that genetic and biological similarities between all forms of life are due to a common Designer who designed similar functions for similar purposes. It doesn’t mean all forms of life are biologically related! Only genetic similarities within a natural species proves relationship because it’s only within a natural species that members can interbreed and reproduce.

Nature cannot build DNA code from scratch. It requires already existing DNA code to direct and bring about more DNA code or a genetic engineer in the laboratory using intelligent design and highly sophisticated technology to bring DNA code into existence from scratch. Furthermore, RNA/DNA and proteins are mutually dependent (one cannot come into existence without the other two) and cannot “survive” or function outside of a complete and living cell. DNA code owes its existence to the first Genetic Engineer – God!

Protein molecules require that various amino acids come together in a precise sequence, just like the letters in a sentence. If they’re not in the right sequence the protein won’t function. DNA and RNA require for various their various nucleic acids to be in the right sequence.

Furthermore, there are left-handed and right-handed amino acids and there are left-handed and right-handed nucleic acids. Protein molecules require for all their amino acids to be left-handed only and in the right sequence. DNA and RNA require for all their nucleic acids to be right-handed and in the right sequence. It would take a miracle for DNA, RNA, and proteins to arise by chance!

Mathematicians have said any event in the universe with odds of 10 to 50th power or greater is impossible! The probability of just an average size protein molecule (with its amino acids in the right sequence) arising by chance is 10 to the 65th power. Even the simplest cell is made up of many millions of various protein molecules along with and DNA/RNA..

The late great British scientist Sir Frederick Hoyle calculated that the odds of even the simplest cell coming into existence by chance is 10 to the 40,000th power! How large is this? Consider that the total number of atoms in our universe is 10 to the 82nd power.

Also, so-called “Junk DNA” isn’t junk. Although these “non-coding” segments of DNA don’t code for proteins, they have recently been found to be vital in regulating gene expression (i.e. when, where, and how genes are expressed, so they’re not “junk”). Also, there is evidence that, in certain situations, they can code for proteins through the cell’s use of a complex “read-through” mechanism.

Visit my latest Internet site: THE SCIENCE SUPPORTING CREATION (This site answers many arguments, both old and new, that have been used by evolutionists to support their theory)

Author of the popular Internet article, TRADITIONAL DOCTRINE OF HELL EVOLVED FROM GREEK ROOTS

*I have given successful lectures (with question and answer period afterwards) defending creation before evolutionist science faculty and students at various colleges and universities. I’ve been privileged to be recognized in the 24th edition of Marquis “Who’s Who in The East.”

This sounds like it could lead to a cure for the rare fatal genetic disease that my grandson has. He is 6 years old and has GM1 type 2. Please get all the links worked out. And cure these precious children of ours. Prayers science cones through for us asap before we lose my grandson.

Can this technology be used to make Vaccines hopefully without any side effects — such as a 100% Successful Side Effect Free Covid19 Vaccine!?

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An on-off switch for gene editing

Over the past decade, the CRISPR-Cas9 gene editing system has revolutionized genetic engineering, allowing scientists to make targeted changes to organisms' DNA. While the system could potentially be useful in treating a variety of diseases, CRISPR-Cas9 editing involves cutting DNA strands, leading to permanent changes to the cell's genetic material.

Now, in a paper published online in Cell on April 9, researchers describe a new gene editing technology called CRISPRoff that allows researchers to control gene expression with high specificity while leaving the sequence of the DNA unchanged. Designed by Whitehead Institute Member Jonathan Weissman, University of California San Francisco assistant professor Luke Gilbert, Weissman lab postdoc James Nuñez and collaborators, the method is stable enough to be inherited through hundreds of cell divisions, and is also fully reversible.

"The big story here is we now have a simple tool that can silence the vast majority of genes," says Weissman, who is also a professor of biology at MIT and an investigator with the Howard Hughes Medical Institute. "We can do this for multiple genes at the same time without any DNA damage, with great deal of homogeneity, and in a way that can be reversed. It's a great tool for controlling gene expression."

The project was partially funded by a 2017 grant from the Defense Advanced Research Projects Agency to create a reversible gene editor. "Fast forward four years [from the initial grant], and CRISPRoff finally works as envisioned in a science fiction way," says co-senior author Gilbert. "It's exciting to see it work so well in practice."

The classic CRISPR-Cas9 system uses a DNA-cutting protein called Cas9 found in bacterial immune systems. The system can be targeted to specific genes in human cells using a single guide RNA, where the Cas9 proteins create tiny breaks in the DNA strand. Then the cell's existing repair machinery patches up the holes.

Because these methods alter the underlying DNA sequence, they are permanent. Plus, their reliance on "in-house" cellular repair mechanisms means it is hard to limit the outcome to a single desired change. "As beautiful as CRISPR-Cas9 is, it hands off the repair to natural cellular processes, which are complex and multifaceted," Weissman says. "It's very hard to control the outcomes."

That's where the researchers saw an opportunity for a different kind of gene editor -- one that didn't alter the DNA sequences themselves, but changed the way they were read in the cell.

This sort of modification is what scientists call "epigenetic" -- genes may be silenced or activated based on chemical changes to the DNA strand. Problems with a cell's epigenetics are responsible for many human diseases such as Fragile X syndrome and various cancers, and can be passed down through generations.

Epigenetic gene silencing often works through methylation -- the addition of chemical tags to to certain places in the DNA strand -- which causes the DNA to become inaccessible to RNA polymerase, the enzyme which reads the genetic information in the DNA sequence into messenger RNA transcripts, which can ultimately be the blueprints for proteins.

Weissman and collaborators had previously created two other epigenetic editors called CRISPRi and CRISPRa -- but both of these came with a caveat. In order for them to work in cells, the cells had to be continually expressing artificial proteins to maintain the changes.

"With this new CRISPRoff technology, you can [express a protein briefly] to write a program that's remembered and carried out indefinitely by the cell," says Gilbert. "It changes the game so now you're basically writing a change that is passed down through cell divisions -- in some ways we can learn to create a version 2.0 of CRISPR-Cas9 that is safer and just as effective, and can do all these other things as well."

To build an epigenetic editor that could mimic natural DNA methylation, the researchers created a tiny protein machine that, guided by small RNAs, can tack methyl groups onto specific spots on the strand. These methylated genes are then "silenced," or turned off, hence the name CRISPRoff.

Because the method does not alter the sequence of the DNA strand, the researchers can reverse the silencing effect using enzymes that remove methyl groups, a method they called CRISPRon.

As they tested CRISPRoff in different conditions, the researchers discovered a few interesting features of the new system. For one thing, they could target the method to the vast majority of genes in the human genome -- and it worked not just for the genes themselves, but also for other regions of DNA that control gene expression but do not code for proteins. "That was a huge shock even for us, because we thought it was only going to be applicable for a subset of genes," says first author Nuñez.

Also, surprisingly to the researchers, CRISPRoff was even able to silence genes that did not have large methylated regions called CpG islands, which had previously been thought necessary to any DNA methylation mechanism.

"What was thought before this work was that the 30 percent of genes that do not have a CpG island were not controlled by DNA methylation," Gilbert says. "But our work clearly shows that you don't require a CpG island to turn genes off by methylation. That, to me, was a major surprise."

CRISPRoff in research and therapy

To investigate the potential of CRISPRoff for practical applications, the scientists tested the method in induced pluripotent stem cells. These are cells that can turn into countless cell types in the body depending on the cocktail of molecules they are exposed to, and thus are powerful models for studying the development and function of particular cell types.

The researchers chose a gene to silence in the stem cells, and then induced them to turn into nerve cells called neurons. When they looked for the same gene in the neurons, they discovered that it had remained silenced in 90 percent of the cells, revealing that cells retain a memory of epigenetic modifications made by the CRISPRoff system even as they change cell type.

They also selected one gene to use as an example of how CRISPRoff might be applied to therapeutics: the gene that codes for Tau protein, which is implicated in Alzheimer's disease. After testing the method in neurons, they were able to show that using CRISPRoff could be used to turn Tau expression down, although not entirely off. "What we showed is that this is a viable strategy for silencing Tau and preventing that protein from being expressed," Weissman says. "The question is, then, how do you deliver this to an adult? And would it really be enough to impact Alzheimer's? Those are big open questions, especially the latter."

Even if CRISPRoff does not lead to Alzheimer's therapies, there are many other conditions it could potentially be applied to. And while delivery to specific tissues remains a challenge for gene editing technologies such as CRISPRoff, "we showed that you can deliver it transiently as a DNA or as an RNA, the same technology that's the basis of the Moderna and BioNTech coronavirus vaccine," Weissman says.

Weissman, Gilbert, and collaborators are enthusiastic about the potential of CRISPRoff for research as well. "Since we now can sort of silence any part of the genome that we want, it's a great tool for exploring the function of the genome," Weissman says.

Plus, having a reliable system to alter a cell's epigenetics could help researchers learn the mechanisms by which epigenetic modifications are passed down through cell divisions. "I think our tool really allows us to begin to study the mechanism of heritability, especially epigenetic heritability, which is a huge question in the biomedical sciences," Nuñez says.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.


SEXUAL REPRODUCTION

Many organisms that can reproduce asexually can also reproduce sexually. Bacteria and other single-celled organisms can also reproduce via a process called conjugation in which the genetic material of two individual cells is reshuffled to produce a third, new individual with a different set of genes than either of its parents. Plants, insects (such as aphids), and other animals (such as starfish), also reproduce sexually by producing sex cells, or gametes, which have only the same number of chromosomes as a normal cell. Gametes are produced in a process called meiosis, in which the pairs of chromosomes that typically inhabit each cell are split in half with each half being distributed to a new cell. Cells with half the normal number of chromosomes are called haploid cells. Sperm and eggs are the human versions of gametes. When two haploid cells merge, as they do in sexual reproduction, the result is a cell with two sets of chromosomes, just like most other cells.

Sexual reproduction is defined as including those processes that result in offspring whose genetic makeup differs from either parent. Sexual reproduction is often slower and more difficult than asexual reproduction and thus does not benefit small populations under difficult circumstances. Sexual reproduction does, however, have the advantage of producing genetic variety and renewal in populations, permitting bad genes to be eliminated and useful genes to be propagated by natural selection.

Sexual reproduction involves the fusing of two gametes. How those gametes get together occurs through a large variety of mechanisms and depends upon a number of factors, including hormones to help individuals produce gametes, the timing of fertilization, and how rich the environment is in which individuals try to survive. Many organisms, especially those living in aquatic environments such as fish, accomplish the fusion of gametes (eggs from females, sperm from males) outside of their bodies in the water. Females deposit eggs and males swim past the eggs releasing sperm into the water. Plants distribute sperm or pollen by means of a number of different vectors including insects, the wind, and birds, depositing it on the stamens of other plants of the same species. In many species, including reptiles and mammals, the male deposits sperm directly into the reproductive organs of the female during a process called sexual intercourse. The gametes fuse inside the female's body and then in some species emerge as eggs (as with birds) in a process called oviparity, or develop inside the mother's body with no connection to the mother as with guppies or snakes (called ovoviviparity), or in others as fetuses to a gestation site on the mother's body (as with marsupials), or are connected to the mother via a placenta in an organ called the uterus as with mammals.

When sperm and egg merge in sexual reproduction, they form a single cell called a zygote with genetic information from both parents. This zygote begins to split and multiply through mitosis into more cells through a process called cleavage. Cell cleavage forms a hollow ball of cells called a blastula, which begins the process of cell differentiation into three layers of cells, which will ultimately form the various organs, tissues, and structures of the fetus. These layers continue to differentiate through a process called organogenesis. One layer, the ectoderm, will form the skin, nervous system, and pituitary gland. The second, the mesoderm, will form the skeleton, muscles, circulatory system, bowels and bladder, and the reproductive organs. The third, the endoderm, forms the liver and the linings of most of the body's internal systems.

After a period of gestation inside the mother's body during which the single-celled zygote grows into a fully formed organism with gametes of its own, the fetus is born. Some infant species are almost completely able to care for themselves. Others, such as most birds and mammals, require an additional period of development and care. Most of these species require additional growth and development before they are able to reproduce in turn.


Regeneration and Polyploidy

Stentor is known for its amazing ability to regenerate. If its body is cut into many small pieces (anywhere from 64 to 100 segments, according to different sources), each piece can produce an entire Stentor. The piece must contain a portion of the macronucleus and the cell membrane in order to regenerate. This is not as unlikely a condition as it may sound. The macronucleus extends through the whole length of the cell and a membrane covers the entire cell.

The macronucleus exhibits polyploidy. The term “ploidy” means the number of sets of chromosomes in a cell. Human cells are diploid because they have two sets. Each of our chromosomes contains a partner bearing genes for the same characteristics. The Stentor macronucleus contains so many copies of chromosomes or segments of chromosomes (tens of thousands or higher, according to various researchers) that it&aposs highly likely that a small piece will contain the necessary genetic information to create a new individual.

Scientists have also observed that a Stentor has an amazing ability to repair damage to the cell membrane. The organism survives wounds that would most likely kill other ciliates and single-celled organisms. The cell membrane is often repaired and life appears to go on as normal for an injured Stentor, even when it has lost some of its internal contents through a wound.


The genetic code is the information for linking amino acids into polypeptides in an order based on the base sequence of 3-base code words (codons) in a gene and its messenger RNA (mRNA). With a few exceptions (some prokaryotes, mitochondria, chloroplasts), the genetic code is universal &ndash it&rsquos the same in all organisms from viruses and bacteria to humans. The table of the Standard Universal Genetic Code on the next page shows the RNA version of triplet codons and their corresponding amino acids. There is a single codon for two amino acids (methionine and tryptophan), but two or more codons for each of the other 18 amino acids. For the latter reason, we say that the genetic code is degenerate. The three stop codons in the Standard Genetic Code &lsquotell&rsquo ribosomes the location of the last amino acid to add to a polypeptide. The last amino acid itself can be any amino acid consistent with the function of the polypeptide being synthesized. However, evolution has selected AUG as the start codon for all polypeptides, regardless of function, as well as for the placement of methionine within a polypeptide. Thus, all polypeptides begin life with a methionine at their amino-terminal end. As we will see in more detail, the mRNA translation machine is the ribosome and the decoding device is tRNA. Each amino acid attaches to a tRNA whose short sequence contains a 3-base anticodon that is complementary to an mRNA codon. Enzymatic reactions catalyze the dehydration synthesis (condensation) reactions that link amino acids in peptide bonds in the order specified by codons in the mRNA.

The near-universality of the genetic code from bacteria to humans implies that the code originated early in evolution. It is probable that portions of the code were in place even before life began. Once in place however, the genetic code was highly constrained against evolutionary change. The degeneracy of the genetic code enabled and contributed to this constraint by permitting base many base changes that do not affect the amino acid encoded in a codon.

The near universality of the genetic code and its resistance to change are features of our genomes that allow us to compare gene and other DNA sequences to establish evolutionary relationships between organisms (species), groups of organisms (genus, family, order, etc.) and even individuals within a species.

In addition to constraints imposed by a universal genetic code, some organisms show codon bias, a recent constraint on which universal codons an organism uses. Codon bias is seen in organisms preferably use A-T rich codons, or in organisms that favor codons richer in G and C. Interestingly, codon bias in genes often accompanies corresponding genomic nucleotide bias. An organism with an AT codon bias may also have an AT-rich genome (likewise GC-rich codons in GC-rich genomes). You can recognize genome nucleotide bias in Chargaff&rsquos base ratios!

Finally, we often think of genetic information as genes for proteins. Obvious examples of non-coding genetic information include the genes for rRNAs and tRNAs, common to all organisms. The amount of these kinds of informational DNA (i.e., genes for polypeptides, tRNAs and rRNAs) as a proportion of total DNA can range across species, although it is higher in eukaryotes prokaryotes. For example,

88% of the E. coli circular chromosome encodes polypeptides, while that figure is less


Structure of DNA

The building blocks of DNA are nucleotides. The important components of each nucleotide are a nitrogenous base, deoxyribose (5-carbon sugar), and a phosphate group (see Figure 2). Each nucleotide is named depending on its nitrogenous base. The nitrogenous base can be a purine, such as adenine (A) and guanine (G), or a pyrimidine, such as cytosine (C) and thymine (T). Uracil (U) is also a pyrimidine (as seen in Figure 2), but it only occurs in RNA, which we will talk more about later.

Figure 2. Each nucleotide is made up of a sugar, a phosphate group, and a nitrogenous base. The sugar is deoxyribose in DNA and ribose in RNA.

The nucleotides combine with each other by covalent bonds known as phosphodiester bonds or linkages. The phosphate residue is attached to the hydroxyl group of the 5&prime carbon of one sugar of one nucleotide and the hydroxyl group of the 3&prime carbon of the sugar of the next nucleotide, thereby forming a 5&prime-3&prime phosphodiester bond.

In the 1950s, Francis Crick and James Watson worked together to determine the structure of DNA at the University of Cambridge, England. Other scientists like Linus Pauling and Maurice Wilkins were also actively exploring this field. Pauling had discovered the secondary structure of proteins using X-ray crystallography. In Wilkins&rsquo lab, researcher Rosalind Franklin was using X-ray diffraction methods to understand the structure of DNA. Watson and Crick were able to piece together the puzzle of the DNA molecule on the basis of Franklin&rsquos data because Crick had also studied X-ray diffraction (Figure 3). In 1962, James Watson, Francis Crick, and Maurice Wilkins were awarded the Nobel Prize in Medicine. Unfortunately, by then Franklin had died, and Nobel prizes are not awarded posthumously.

Figure 3. The work of pioneering scientists (a) James Watson, Francis Crick, and Maclyn McCarty led to our present day understanding of DNA. Scientist Rosalind Franklin discovered (b) the X-ray diffraction pattern of DNA, which helped to elucidate its double helix structure. (credit a: modification of work by Marjorie McCarty, Public Library of Science)

Watson and Crick proposed that DNA is made up of two strands that are twisted around each other to form a right-handed helix. Base pairing takes place between a purine and pyrimidine namely, A pairs with T and G pairs with C. Adenine and thymine are complementary base pairs, and cytosine and guanine are also complementary base pairs. The base pairs are stabilized by hydrogen bonds adenine and thymine form two hydrogen bonds and cytosine and guanine form three hydrogen bonds. The two strands are anti-parallel in nature that is, the 3&prime end of one strand faces the 5&prime end of the other strand. The sugar and phosphate of the nucleotides form the backbone of the structure, whereas the nitrogenous bases are stacked inside. Each base pair is separated from the other base pair by a distance of 0.34 nm, and each turn of the helix measures 3.4 nm. Therefore, ten base pairs are present per turn of the helix. The diameter of the DNA double helix is 2 nm, and it is uniform throughout. Only the pairing between a purine and pyrimidine can explain the uniform diameter. The twisting of the two strands around each other results in the formation of uniformly spaced major and minor grooves (Figure 4).

Figure 4. DNA has (a) a double helix structure and (b) phosphodiester bonds. The (c) major and minor grooves are binding sites for DNA binding proteins during processes such as transcription (the copying of RNA from DNA) and replication.


Chromosomal Abnormalities and Gene Mutation

Although DNA replications are mostly accurate, there are times when errors in replication occur, owing to alterations in the base gene sequence. These errors give rise to what is known as mutations. Changes in the chromosomal content of a cell, including errors in replication, DNA, and gene mutations can give rise to a number of medical conditions, like Down Syndrome. This does not mean that all chromosomal abnormalities will give rise to a disease. However, a parent with chromosomal abnormalities has higher chances of giving birth to a child with genetic disorders. There is hope though, with advances in genetic engineering for people with such conditions.

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The functions carried out by chromosomes form the very basis of life and its continuity. Chromosomes and genes are just the tip of the iceberg under the fascinating subject of genetics. They are being studied for decades to understand the makeup of human, animal, and plant structures. Genetics reveal the causes of ailments and disorders and also provide for their solution.

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