Using the information provided in this article, calculate the number of
mouse and human genes that are the same or similar.
This is only done for the antibodies corresponding to genes where
the mouse and human genes are orthologous.
The catalog of
mouse and human genes yielded by these genome projects will cut years of time from otherwise painstaking laboratory research.
Not exact matches
Infant formula continues to evolve
and there are patents already for implanting
genes for making
human milk in
mice.
As part of the study, researchers found that
mice engineered to develop symptoms of
human inflammatory disease,
and which also lacked the ATG16L1
gene, developed gut damage.
Until now, roughly 150 imprinted
genes have been found in
mice and about half that number in
humans.
Both
mouse and human males typically die early from the mutation in Mecp2, because their Y chromosome does not supply a normal copy of the
gene.
Researchers at Weill Cornell Medical College recently identified a
gene abnormality that is associated with anxiety - related behaviors; it makes
humans and mice hypervigilant to cues that signal danger.
Humans and mice share about 97 percent of their
genes.
These four
genes and their proteins constitute the heart of the biological clock in flies,
and with some modifications they appear to form a mechanism governing circadian rhythms throughout the animal kingdom, from fish to frogs,
mice to
humans.
In a test of this theory, researchers have demonstrated that
mice harboring a
human SCN1A
gene mutation that results in Dravet Syndrome (DS), a severe
and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation
and sudden cardiac death.
In today's issue of Cell, a team reports that it has found in
mice and humans a close relative of a fruit fly clock
gene — the first evidence that some of these
genes may have been conserved over the course of evolution.
This consortium selected 44 separate sections of the genome that included regions of high to low
gene density
and high to low similarity between
mouse and human.
The researchers have compared various processes involved in
gene expression, such as
gene transcription
and chromatin modification,
and have repeated this in different tissues
and cell types from both
humans and mice.
Like the per
gene, the new
genes — dubbed RIGUI in
humans and m - rigui in
mice — are turned on
and off in a daily cycle
and may work with other
genes to generate the oscillating mechanism that runs the internal clock.
In addition, the researchers have quantified the preservation level of this
gene expression between
humans and mice.
Molecular geneticist Cheng Chi Lee, developmental biologist Gregor Eichele,
and their co-workers at the Baylor College of Medicine in Houston have isolated a
gene in
mice and humans that shares 44 % of the amino acid sequence of the period (per)
gene of the fruit fly Drosophila melanogaster.
The UT Southwestern group had previously used CRISPR - Cas9, the original
gene - editing system, to correct the Duchenne defect in a
mouse model of the disease
and in
human cells.
An additional study, currently available at bioRxiv, led by the researchers from the CRG
and Cold Spring Harbour Laboratory, highlights the fact that a substantial part of
human and mice genes have maintained an essentially constant expression throughout evolution, in tissues
and various organs.
The IGF1 protein is crucial for the growth of mammals, including
mice and humans, so Ostrander's group
and other collaborators began collecting DNA from additional breeds to see if they also shared the same
gene variant.
Many universities
and pharmaceutical companies are engaged in research
and development using genetically modified
mice that have certain
genes manipulated to reproduce
human diseases.
When we took the
mouse version of this
gene — the same
gene we find in the
human —
and put it in the fly
and tweaked it, we induced fly eye tissue.
The
human (
and all the other) genome projects were predicated on the reasonable assumption that spelling out the full sequence of
genes would reveal the source of that diversity of form
and attributes that so readily distinguish worm from fly,
mouse, chimp
and human.
Using the new
gene - editing enzyme CRISPR - Cpf1, researchers at UT Southwestern Medical Center have successfully corrected Duchenne muscular dystrophy in
human cells
and mice in the lab.
The loss of a single
gene in
mice can affect social behavior
and impair their brains» ability to filter out distractions — both characteristics of several neurological diseases in
humans.
Already, researchers have used CRISPR / Cas9 to edit
genes in
human cells grown in lab dishes, monkeys (SN: 3/8/14, p. 7), dogs (SN: 11/28/15, p. 16),
mice and pigs (SN: 11/14/15, p. 6), yeast, fruit flies, the worm Caenorhabditis elegans, zebrafish, tobacco
and rice.
In the current work, they used a new variation of the
gene - editing system to repair the defect in both a
mouse model
and in
human cells.
To see if they would suffice to make H5N1 infection less severe, Webby
and his co-workers injected
mice with DNA for the neuraminidase
gene from
human H1N1, one of three flu subtypes covered by this winter's flu shot.
Mice without the leptin
gene, called ob / ob, overeat, weigh in at three to four times normal,
and develop symptoms similar to the obesity - related diabetes seen in
humans.
Compared with earlier methods to tweak the genomes of bacteria, plants, laboratory
mice and human cells, the Crispr - Cas9
gene - editing method is fast, precise
and cheap, an order of magnitude better than the others.
All animals use the same enzyme to create the same methylation mark as a signal for
gene repression,
and her colleagues who study epigenetics in
mice and humans are excited about the new findings, Strome said.
A screen for
mouse genes dependent on dHAND, a transcription factor implicated in neural crest development, identified Ufd1, which maps to
human 22q11
and encodes a protein involved in degradation of ubiquitinated proteins.
By comparing our genetic make - up to the genomes of
mice, chimps
and a menagerie of other species (rats, chickens, dogs, pufferfish, the microscopic worm Caenorhabditis elegans, the fruit fly Drosophila melanogaster
and many bacteria), scientists have learned a great deal about how
genes evolve over time,
and gained insights into
human diseases.
These are not
genes but must have an important role because evolution has left them virtually unchanged in both
humans and mice since our evolutionary paths parted about 75 million years ago.
However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single
gene, according to a study that found that restoring normal levels of a
human colorectal cancer
gene in
mice stopped tumor growth
and re-established normal intestinal function within only 4 days.
The group has already started tweaking
human iPS cells using the same
genes that Saitou pinpointed as being important in
mouse germ - cell development, but both Saitou
and Hayashi know that
human signalling networks are different from those in
mice.
In
humans and mice, the
gene is associated with height, face development
and other traits.
The problem is that in animals, such as
mice and humans, there are many histone
genes and they are scattered throughout the genome.
One
gene, which codes for a powerful growth - stimulating hormone in
mice and humans, is expressed only by paternally derived
genes.
Before Katlyn showed up at NIH, the doctors there were already well prepared: They had inserted healthy
human ADA
genes into a modified
mouse retrovirus — a type of virus that can enter
human cells
and transfer new genetic material right into the DNA strands in their nuclei.
We currently produce DNA microarrays representing the yeast,
mouse,
and human genomes (the yeast microarray has over 6000 yeast
genes, the
mouse microarray has over 15,000
mouse genes,
and the two
human microarrays have 1700
genes and over 19,000
genes).
Two recent studies — one in
mice and another in
humans — provide new evidence that a mind - numbingly complex array of
genes influence body weight.
Although that marker, called IL21, had not previously been associated with autoimmune diseases, the
gene that produces it sits right in the stretch of DNA known to make these
mice vulnerable to diabetes, suggesting that IL21 might make a drug target, says Sarvetnick.Furthermore, by giving the animals a shot of dead bacteria — similar to an immunization in
humans — when they were newborns, Sarvetnick
and her colleagues prevented a surfeit of CD4 +
and CD8 + cells.
Now, a new study in
mice shows how a
gene, called FOXP2, implicated in a language disorder may have changed between
humans and chimps to make learning to speak possible — or at least a little easier.
Early in embryonic development, both
mouse and human placentas rely on the same set of ancient cell - growth
genes.
Buxbaum
and his coworkers point out that FOXP2 is also expressed in the brains of songbirds such as finches
and canaries,
and further studies of the
gene in
mice might provide a better understanding of its role in
human communication.
Fittingly, most of these
genes reside in ampliconic regions of the X
and appear to have been acquired independently during the 80 million years since
mouse and human diverged from a common ancestor.
By studying how these
genes cause defects in fly
and mouse models, we can improve our insights into the mechanisms related to
human disease,» said corresponding author
and Dr. Hugo J. Bellen, professor of neuroscience
and molecular
and human genetics at Baylor College of Medicine
and an investigator at the Howard Hughes Medical Institute.
Although the
gene / cell therapy strategy was highly successful in laboratory
mice, the authors stressed that additional research
and testing are needed before the therapy could be tested in
humans.
Such
genes play an important role in mate selection — not just in bats, but also in
mice and possibly even
humans.