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Model baru untuk evolusi bisa ular
Para peneliti telah menemukan bukti genetik bahwa protein racun yang sangat beracun yang evolusioner ' lahir ' dari gen non - toksik , yang memiliki pekerjaan biasa lainnya di seluruh tubuh , seperti regulasi fungsi seluler atau pencernaan makanan .....read more
New model for snake venom evolution
proposed
Date:
December 8, 2014
Source:
University of Texas at Arlington
Summary:
Researchers have found genetic evidence that highly toxic venom proteins
were evolutionarily 'born' from non-toxic genes, which have other ordinary jobs
around the body, such as regulation of cellular functions or digestion of food.
.........................
Technology that can map out the genes at work in a snake or lizard's mouth
has, in many cases, changed the way scientists define an animal as venomous. If
oral glands show expression of some of the 20 gene families associated with
"venom toxins," that species gets the venomous label.
But, a new study from The University of Texas at Arlington challenges that
practice, while also developing a new model for how snake venoms came to be.
The work, which is being published in the journal Molecular Biology and
Evolution, is based on a painstaking analysis comparing groups of related
genes or "gene families" in tissue from different parts of the
Burmese python, or Python molurus bivittatus.
A team led by assistant professor of biology Todd Castoe and including
researchers from Colorado and the United Kingdom found similar levels of these
so-called toxic gene families in python oral glands and in tissue from the
python brain, liver, stomach and several other organs. Scientists say those
findings demonstrate much about the functions of venom genes before they
evolved into venoms. It also shows that just the expression of genes related to
venom toxins in oral glands of snakes and lizards isn't enough information to
close the book on whether something is venomous.
"Research on venom is widespread because of its obvious importance to
treating and understanding snakebite, as well as the potential of venoms to be
used as drugs, but, up until now, everything was focused in the venom gland,
where venom is produced before it is injected," Castoe said. "There
was no examination of what's happening in other parts of the snake's body. This
is the first study to have used the genome to look at the rest of that
picture."
Learning more about venom evolution could help scientists develop better
anti-venoms and contribute to knowledge about gene evolution in humans
Castoe said that with an uptick in genetic analysis capabilities,
scientists are finding more evidence for a long-held theory. That theory says
highly toxic venom proteins were evolutionarily "born" from non-toxic
genes, which have other ordinary jobs around the body, such as regulation of
cellular functions or digestion of food.
"These results demonstrate that genes or transcripts which were
previously interpreted as 'toxin genes' are instead most likely housekeeping
genes, involved in the more mundane maintenance of normal metabolism of many
tissues," said Stephen Mackessy, a co-author on the study and biology
professor at the University of Northern Colorado. "Our results also
suggest that instead of a single ancient origin, venom and venom-delivery
systems most likely evolved independently in several distinct lineages of
reptiles."
Castoe was lead author on a 2013 study that mapped the genome of the
Burmese python. Pythons are not considered venomous even though they have some
of the same genes that have evolved into very toxic venoms in other species.
The difference is, in highly venomous snakes, such as rattlesnakes or cobras,
the venom gene families have expanded to make many copies of those shared
genes, and some of these copies have evolved into genes that produce highly
toxic venom proteins.
"The non-venomous python diverged from the snake evolutionary tree
prior to this massive expansion and re-working of venom gene families.
Therefore, the python represents a window into what a snake looked like before
venom evolved," Castoe said. "Studying it helps to paint a picture of
how these gene families present in many vertebrates, including humans, evolved
into deadly toxin encoding genes."
Jacobo Reyes-Velasco, a graduate student from Castoe's lab, is lead author
on the new paper. In addition to Castoe and Mackessy, other co-authors are:
Daren Card, Audra Andrew, Kyle Shaney, Richard Adams and Drew Schield, all from
the UT Arlington Department of Biology; and Nicholas Casewell, of the Liverpool
School of Tropical Medicine.
The paper is titled "Expression of Venom Gene Homologs in Diverse
Python Tissues Suggests a New Model for the Evolution of Snake Venom."
The research team looked at 24 gene families that are shared by pythons,
cobras, rattlesnakes and Gila monsters, and associated with venom. The traditional
view of venom evolution has been that a core venom system developed at one
point in the evolution of snakes and lizards, referred to as the Toxicofera,
and that the evolution of highly venomous snakes, known as caenophidian snakes,
came afterward. But little explanation has been given for why evolution picked
just 24 genes to make into highly toxic venom-encoding genes, from the 25,000
or so possible.
"We believe that this work will provide an important baseline for
future studies by venom researchers to better understand the processes that
resulted in the mixture of toxic molecules that we observe in venom, and to
define which molecules are of greatest importance for killing prey and causing
pathology in human snakebite victims," Casewell said.
When they looked at the python, the team found several common
characteristics among the venom-related gene families that differed from other
genes. Compared with other python gene families, venom gene families are
"expressed at lower levels overall, expressed at moderate-high levels in
fewer tissues and show among the highest variation in expression level across
tissues," Castoe said.
"Evolution seems to have chosen what genes to evolve into venoms based
on where they were expressed (or turned on), and at what levels they were
expressed," Castoe said.
Based on their data, the new paper presents a model with three steps for
venom evolution. First, these potentially venomous genes end up in the oral
gland by default, because they are expressed in low but consistent ways
throughout the body. Then, because of natural selection on this expression in
the oral gland being beneficial, tissues in the mouth begin expressing those
genes in higher levels than in other parts of the body. Finally, as the venom
evolves to become more toxic, the expression of those genes in other organs is
decreased to limit potentially harmful effects of secreting such toxins in
other body tissues.
The team calls its new model the Stepwise Intermediate Nearly Neutral
Evolutionary Recruitment, or SINNER, model. They say differing venom levels in
snakes and other animals could be traced to the variability of where different
species, or different genes within a species, are along the continuum between
the beginning and end of the SINNER model.
Castoe said the next step in the research would be to examine the genome of
highly venomous snakes to see if the SINNER model bears out. For now, he and
the rest of the team hope that their findings about the presence of
venom-related genes in other parts of the python change some thinking on what
species are labeled as venomous.
"What is a venom and what species are venomous will take a lot more
evidence to convince people now," Castoe said. "It provides a brand
new perspective on what we should think of when we look at those oral
glands."
Story Source:
The above story is based on materials provided
by University of Texas at Arlington. Note:
Materials may be edited for content and length.
Journal Reference:
1.
J. Reyes-Velasco, D. C. Card, A. L. Andrew, K. J. Shaney, R. H. Adams, D.
R. Schield, N. R. Casewell, S. P. Mackessy, T. A. Castoe. Expression of
Venom Gene Homologs in Diverse Python Tissues Suggests a New Model for the
Evolution of Snake Venom. Molecular Biology and Evolution,
2014; DOI: 10.1093/molbev/msu294