A RESEARCH ON GENOMIC IMPRINTING Genomic imprinting is the epigenetic phenomenon mostly occurring in gametogenesis. It has independently evolved in flowering plants and mammals. In both organisms, imprinting occurs in the embryo-nourishing tissues; the endosperm and the placenta respectively. Imprinting genes regulate the transfer of nutrients to developing progeny (Beery & Workman, 2011).The genomic imprinting usually occurs when both the maternal and the paternal alleles are present but one allele expresses itself while the other remains inactive ( Engel, N. 2015). Gene imprinting is believed to be important in regulation of growth in embryo and neonate Experiments on androgenotes and gynogenotes , which are produced by nuclear transplantation, are used to create basis of genomic imprinting. The zygotes from androgenotes and gynogenotes were formed but neither type could undergo more development. From this situation, it is possible to suggest that the maternal and paternal effects are complimentary(Morgan, Li, & O’Neill, 2009). Each genome contains different viable and necessary properties. Another evidence that genomic imprinting has a major role in growth and development comes from a research by Li et al(1993). Optimal method for gene imprinting is DNA methylation, which is carried out with enzyme DNA methyltransferase in mammals. DNA MTase acts on the DNA sequence 5’-6pG-3’. Primarily higher eukaryotes have CpG islands in their genomes. The islands are hardly methylated in the animal cells, this could be due to the bound transcription factors that block DNA MTase. Those sequences which are methylated are normally not active. Some research also show that methylated sequences can be active (Madek, 1974). The importance of DNA methylation was demonstrated in the study of mammalian development(Li et al, 1993). They postulated that if mutation was introduced to the DNA MTase gene in embryonic stem cell of a mice, methylation of CpG would be abnormal and the gene expression would be affected (“DNA methylation and demethylation dynamics,” 2015). Gene mutation of DNA MTase was caused by homologous recombination and Southern blot analysis affirmed this (Wilkins, 2010). The genes used were insulin-like growth factors; H19, lgf2 and lgf2 receptor; lgf2r. Normally H19 gene, whih is a maternal allele, is expressed while the paternal allele is inactive. Inactive paternal allele is methylated but the maternal allele is not; this should be noted carefully. RNase and Northern blot analysis essays procedures demonstrated the effects of decreased levels of DNA methylation on mutant mice. It was brought to light that typical DNA methylation is a requirement to keep for the paternal allele inactive for the H19 gene (Mightiness of science, 2016) The lgf2 is opposite of the H19 gene in that it is expressed only in a methylated paternal allele. As a result, it is expressed in mice having deficient MTase activity. It is expected that the lgf2 gene wil.

1. A RESEARCH ON GENOMIC IMPRINTING
Genomic imprinting is the epigenetic phenomenon mostly
occurring in gametogenesis. It has independently evolved in
flowering plants and mammals. In both organisms, imprinting
occurs in the embryo-nourishing tissues; the endosperm and the
placenta respectively. Imprinting genes regulate the transfer of
nutrients to developing progeny (Beery & Workman, 2011).The
genomic imprinting usually occurs when both the maternal and
the paternal alleles are present but one allele expresses itself
while the other remains inactive ( Engel, N. 2015). Gene
imprinting is believed to be important in regulation of growth in
embryo and neonate
Experiments on androgenotes and gynogenotes , which are
produced by nuclear transplantation, are used to create basis of
genomic imprinting. The zygotes from androgenotes and
gynogenotes were formed but neither type could undergo more
development. From this situation, it is possible to suggest that
the maternal and paternal effects are complimentary(Morgan,
Li, & O’Neill, 2009). Each genome contains different viable and
necessary properties. Another evidence that genomic imprinting
has a major role in growth and development comes from a
research by Li et al(1993).
Optimal method for gene imprinting is DNA methylation, which
is carried out with enzyme DNA methyltransferase in
mammals. DNA MTase acts on the DNA sequence 5’-6pG-3’.
Primarily higher eukaryotes have CpG islands in their genomes.
The islands are hardly methylated in the animal cells, this could
be due to the bound transcription factors that block DNA
MTase. Those sequences which are methylated are normally not
active. Some research also show that methylated sequences can
be active (Madek, 1974).

2. The importance of DNA methylation was demonstrated in the
study of mammalian development(Li et al, 1993). They
postulated that if mutation was introduced to the DNA MTase
gene in embryonic stem cell of a mice, methylation of CpG
would be abnormal and the gene expression would be affected
(“DNA methylation and demethylation dynamics,” 2015). Gene
mutation of DNA MTase was caused by homologous
recombination and Southern blot analysis affirmed this
(Wilkins, 2010). The genes used were insulin-like growth
factors; H19, lgf2 and lgf2 receptor; lgf2r.
Normally H19 gene, whih is a maternal allele, is expressed
while the paternal allele is inactive. Inactive paternal allele is
methylated but the maternal allele is not; this should be noted
carefully. RNase and Northern blot analysis essays procedures
demonstrated the effects of decreased levels of DNA
methylation on mutant mice. It was brought to light that typical
DNA methylation is a requirement to keep for the paternal
allele inactive for the H19 gene (Mightiness of science, 2016)
The lgf2 is opposite of the H19 gene in that it is expressed only
in a methylated paternal allele. As a result, it is expressed in
mice having deficient MTase activity. It is expected that the
lgf2 gene will be repressed, while the paternal allele remains
unmethylated. Analysis of 9 day-old embryos using RNase
protection essay examined expression of lgf2 and cytoplasmic
action. Northern blots revealed that in homozygous DNA MTase
mutants, lgf2 was undetectable. From the findings, it was
concluded that a normal level of DNA methylation is needed for
expression of the paternal lgf2 allele.
The gene lgf2r is expressed from a methylated maternal allele.
Predictions were made and found out that MTase-deficient
mutants alleles expressed lgf2r at some level as wild type
alleles. It was suspected by Li et al that the lgf2r gene was

3. significantly less affected by demethylation of genomic DNA
but not independent of it. In order to test this, second MTase
deficient mutant was created that had a deletion downstream
from the first mutant’s deletion. The second deletion caused
deficiencies so severe that embryos died at day 10, forming only
5-10 somites. RNase protection analysis indicated that the
second mutant repressed the expression of the lgf2r gene
completely. The effects of DNA demethylation on maternal
lgf2r allele are substantially less significant than those of
demethylation of the paternal lgf2 allele.
Genomic imprinting has implications in embryonic and extra-
embryonic growth and development in a variety of organisms.
Many experiments have agreed to this including Li et al’s
research. To date, 50 imprinting genes have been identified in
the human genome. The genes tend to be clustered together in
imprinted chromosomal domains. The domains have s been
mapped to chromosomes 7q32, 11p15, 15q11 and 20q13. The
cluster of genes are characterized by cis regulation via IC.
According to AC Smith-2007, dysregulation of this gene cluster
is associated with overgrowth and tumor predisposition
syndrome, Beckwith-Wiedemann syndrome. The disruption of
imprinted gene expression can result from genetic or epigenetic
alteration. The genetic alteration such as duplication, deletion,
translocation, inversion and mutation in imprinted regions have
been shown to cause disease (Committee, Research, &
Organization, 2002). Epimutations that are extrinsic to the
primary DNA sequence have also been shown to cause diseases.
Recently, several human diseases in addition to Beckwith-
Wiedemann syndrome have been reported to have molecular
alterations at chromosome 11p15.5. The diseases include
Russell-silver syndrome and transient neonatal diabetes mellitus
Sluckin, W., & Sluckin, W. (1973). Imprinting and early
learning (2nd ed.). Chicago: Methuen.
Mackay et al (49) suggested that methylation defects at more

4. than one locus can modify the clinical presentation of the
TNDM phenotype. Most of TNDM patients presenting with lose
of methylation at KCNQ1OT1 DMR have macroglossia and
abdominal wall defects commonly seen in BWS patients
(Shomu’s Biology, 2015)
REFERENCES
1. Engel, N. (2015). Genomic imprinting in mammals—
memories of the generations past. Epigenetic Gene Expression
and Regulation, 43-61. doi:10.1016/b978-0-12-799958-6.00003-
2
2. Morgan, H. D., Li, Y., & O’Neill, C. (2009). 127.
EPIGENETIC REPROGRAMMING IN ZYGOTES INVOLVES
THE GLOBAL CYTOSINE DEMETHYLATION OF BOTH THE
PATERNAL AND MATERNAL GENOMES. Reproduction,
Fertility and Development, 21(9), 46. doi:10.1071/srb09abs127
3. Madek, B. E. H. (1974). Sequences of methylated T1 plus
pancreatic ribonuclease products. Journal of Molecular
Biology, 88(1), 158–164. doi:10.1016/0022-2836(74)90301-5
4.
DNA methylation and demethylation dynamics
(2015). Oncotarget. doi:10.18632/oncotarget.6039
5. Beery, T. A., & Workman, L. M. (2011). Genetics and
genomics in nursing and health care. Philadelphia: F.A. Davis
Company.
6. Wilkins, J. F. (2010). GENOMIC IMPRINTING AND
CONFLICT-INDUCED DECANALIZATION.Evolution, 65(2),
537–553. doi:10.1111/j.1558-5646.2010.01147.x
7. Mightiness of science (2016, August 11). Genomic
imprinting Retrieved from https://youtu.be/b7J2gW-GqTw
8. Shomu’s Biology (2015, August 30). Genomic
imprinting Retrieved from https://youtu.be/6xvsyJNphHo
9. Committee, the A., Research, H., & Organization, W. H.
(2002). Genomics and world health: Report of the advisory
committee on health research. Geneva: World Health

5. Organization.
10. Sluckin, W., & Sluckin, W. (1973). Imprinting and early
learning (2nd ed.). Chicago: Methuen.
A RESEARCH ON GENOMIC IMPRINTING
Genomic imprinting is the epigenetic phenomenon mostly
occurring in
gametogenesis. It has
independently evolved in flowering plants and mammals. In
both organisms, imprinting occurs
in the embryo
-
nourishing tissues; the endosperm and the placenta respectively.
Imprinting genes
regulate the transfer of nutrients to develop
ing progeny
(Beery & Workman, 2011)
.
The g
enomic
imprinting
usually
occurs when both

6. the
maternal and
the paternal
alleles are present but one
allele expresses itself while the other remains inactive
( Engel, N. 2015)
. Gene imprinting is
believed to be important in regulation
of growth in embryo and neonate
Experiments on androgenotes and gynogenotes , which are
produced by nuclear transplantation,
are used to create basis of genomic imprinting. The zygotes
from andr
ogenotes and gynogenotes
were for
med but neither type
could undergo
more
development. From this situation, it is possible
to suggest that the maternal and paternal effects a
re complimentary
(Morgan, Li, & O’Neill,
2009)
. Each genome contains different viabl
e and nece
ssary properties.
Another evidence that

7. genomic imprinting has a major role in growth and development
comes from a research by Li et
al(1993).
Optimal method for gene imprinting is DNA methylation, which
is carried out with enzyme
DNA methyltran
sferase in mammals. DNA MTase acts on the DNA sequence 5’
-
6pG
-
3’.
Primarily higher eukaryotes have CpG islands in their genomes.
The islands are hardly
methylated in the animal cells, this could be due to the bound
transcription factors that block
Topic: ANIMAL RESEARCH VS MEDICAL RESEARCH
Style: APA
LENGTH: PART -1 7pages-(2100) words excluding cover page
and references
PART TWO-8 slides presentation.
PLAGIARISM :MUST BE ZERO AND NO GRAMMAR
ERRORS
NB:this is very important to me please don’t disappoint.
Scholarly articles reviews on GENOMIC IMPRINTING
Bartolomei, M. S. (2009). Genomic imprinting: employing and
avoiding epigenetic processes. Genes & development, 23(18),
2124-2133.
Chamberlain, S. J., & Lalande, M. (2010). Angelman syndrome,
a genomic imprinting disorder of the brain. The Journal of
Neuroscience, 30(30), 9958-9963.
Frésard, L., Leroux, S., Servin, B., Gourichon, D., Dehais, P.,
San Cristobal, M., ... & Hormozdiari, F. (2014). Transcriptome-
wide investigation of genomic imprinting in chicken. Nucleic

8. acids research, 42(6), 3768-3782.
Jiang, H., & Köhler, C. (2012). Evolution, function, and
regulation of genomic imprinting in plant seed
development. Journal of experimental botany, 63(13), 4713-
4722.
MacDonald, W. A. (2012). Epigenetic mechanisms of genomic
imprinting: common themes in the regulation of imprinted
regions in mammals, plants, and insects. Genetics research
international, 2012.
O’Doherty, A. M., MacHugh, D. E., Spillane, C., & Magee, D.
A. (2015). Genomic imprinting effects on complex traits in
domesticated animal species. Frontiers in genetics, 6, 156.
Peters, J. (2014). The role of genomic imprinting in biology and
disease: an expanding view. Nature Reviews Genetics, 15(8),
517-530.
Powledge, T. M. (2011). Behavioral epigenetics: how nurture
shapes nature.BioScience, 61(8), 588-592.
Thomsen, P. D. (2007). Genomic imprinting–an epigenetic
regulation of fetal development and loss. Acta Veterinaria
Scandinavica, 49(1), 1.
Tucci, V. (2016). Genomic Imprinting: A New Epigenetic
Perspective of Sleep Regulation. PLoS Genet, 12(5), e1006004.
Topic:
ANIMAL
RESEARCH VS MEDICAL RESEARCH
S
ty
le
:
APA

9. LENGTH
:
PART
-
1
7pages
-
(
2100) words
excluding cover page and
ref
erences
PART TWO
-
8
slides presentation
.
PLAGIARISM :MUST BE ZERO AND NO GRAMMAR
ERRORS
NB:this is very important to me please
don’t
disappoint
.
Scholarly articles reviews on GENOMIC IMPRINTING

10. Bartolomei, M. S. (2009). Genomic imprinting: employing and
avoiding epigenetic
processes.
Genes & development
,
23
(18), 2124
-
2133.
Chamberlain, S. J., & Lalande, M. (2010). Angelman syndrome,
a genomic
imprinting disorder
of the brain.
The Journal of Neuroscience
,
30
(30), 9958
-
9963.
Frésard, L., Leroux, S., Servin, B., Gourichon, D., Dehais, P.,
San Cristobal, M., ... &
Hormozdiari, F. (2014). Transcriptome
-
wide investigation of genomic imprinting in
chicken.
Nucleic acids research
,

11. 42
(6), 3768
-
3782.
Jiang, H., & Köhler, C. (2012). Evolution, function, and
regulation of genomic imprinting in
plant seed development.
Journ
al of experimental botany
,
63
(13), 4713
-
4722.
MacDonald, W. A. (2012). Epigenetic mechanisms of genomic
imprinting: common themes in
the regulation of imprinted regions in mammals, plants, and
insects.
Genetics research
international
,
2012
.
O’Doherty, A.
M., MacHugh, D. E., Spillane, C., & Magee, D. A. (2015).
Genomic imprinting
effects on complex traits in domesticated animal species.

12. Frontiers in genetics
,
6
, 156.