Summary

Introduction
From the very start of the article it has a summary telling us what the researchers are looking for.
When doing present day studies they found that when mice lack either miR-133a-1 and
miR-133a-2 they are completely normal. Whereas if there is just a deletion of the genes thats
when the aberrant expression of smooth muscle genes in the heart shows up.
They chose this topic because they wanted to find out more on what is the difference in having
something be normal or a smooth gene expression of the heart. And it is easier to do all this
testing on mice.
The researches are wanting to gather why this is. First of all they think the heart is fascinating
and wanted to know more. So they used mice for there testers. They want to find out why there is
a difference from lacking the gene completely and just a deletion of the gene.
In the very last sentence of the last paragraph in the Scientist stated that, We conclude that
miR-133a-1 and miR-133a-2 redundantly regulate the gene expression programs required for
normal cardiac growth and function.
Materials and Methods
When looking under the materials and methods section it clearly states many different ways they
went about getting there research for DNA. For this particular experiment they used all different
sorts of things. They did gene targeting and mouse breeding, RNA analysis, Northern blot,
Western blot, Plasmids, cell culture, and luciferase assays, histology, electron microscopy,

immunohistochemistry, transthoratic echocaardioology, statistical analysis, and bioinformatics

and miRNA target analysis.
When performing any of these test on the mice for example they would take samples from the
ventricles and have them processed.
Nothing specifically says that they used nay sort of DNA but it states that they used RNA or
LVID as well as cyclin. They execrate protein from hearts and did standard protocol under the
Western blot.
Results
For the results in the different mice an different kind of tests the scientist found exactly what they
were looking for. While doing just a targeted deletion and using the heterozygous mice it showed
no apparent defects in behavior, weight, or lifespan. Same thing with the mutant mice. In doing
the same test on double- mutant it showed that 50% of mice died.
They weren't expecting as many deaths as they were getting. They were also surprised at a how
well it all these tests were working with the smooth gene muscle experiment on the heart.
Discussion
While looking in the discussion they newt they were doing no doubt. They proved exactly what
they were set out to do. They new what they wanted and had an idea of who to get there an figure
it out. They had a couple different types of mice and ran the same test on them so they could get
the best results.

I think they exhausted this as much as they could have. That may never seem like enough though
to any scientist. Personally I think that they did a good job and had a lot of good information to
work off of and were able to get what they needed in the process.
The Scientists did so much studying and research with this topic and all there mice. They did an
amazing job with everything and proved there point and exactly what they needed too.

Bibliography
Liu, Ning, Svetlana Bezprozvannaya, and Andrew H. Williams. "MicroRNA-133a Regulates
Cardiomyocyte Proliferation and Suppresses Smooth Muscle Gene Expression in the
Heart." MicroRNA-133a Regulates Cardiomyocyte Proliferation and Suppresses Smooth
Muscle Gene Expression in the Heart. N.p., 17 Nov. 2008. Web. 01 Apr. 2016.