Agriculture Reference
In-Depth Information
In contrast to plants, animals usually display a highly determined path
of terminal development reaching a
final adult patterned collection of
somatic cells that are minimally capable of producing new speci
c cells,
tissues, or complex structures by either the presence of stem cells within
adult tissues or by dedifferentiation (Sugimoto et al. 2011). Exceptions
occur generally, or in speci
c species and include horns or antlers, nails,
teeth, hair, skin, blood, muscle, and endothelial cells and in some cases,
complex organs and structures such as liver, bone, spinal cord, tails, and
even limbs. Unlike plants, animal somatic cells have never been
observed to direct the reformation of the complete organism. An early
work with amphibian nuclei implanted into denucleated eggs revealed
that somatic nuclei could retain totipotency but only in the presence of
egg cytoplasm (Briggs and King 1952). As they became increasingly
differentiated, totipotency of somatic nuclei in the presence of egg
cytoplasm decreased (Briggs and King 1952; Fischberg et al. 1958).
The epigenetic awaking has resulted in a better understanding of
several aspects of developmental epigenetics in animals than in plants
(Surani and Reik 2007; Cantone and Fisher 2013). In the last decade,
massive and intense efforts have revealed in animals three basic types of
molecular manipulations that can control both differentiation of pluri-
potent cells and dedifferentiation of terminal somatic cells, nuclear
reprogramming, nuclear transfer, and appropriate transcription factor
transduction (Yamanaka and Blau 2010; Dejosez and Zwaka 2012). All
are capable of producing extensive epigenetic restructuring to accom-
plish amazing cell-type transformations. These astonishing achieve-
ments appear to be the result of
“
tipping the balance
”
of key
ontogenic signal factors (Yamanaka and Blau 2010).
In mammals, it has been demonstrated that although epigenetic mark
resetting can occur in gametogenesis, major resetting takes place during
a very short period in an early embryo stage creating a narrow trans-
generational window that is vulnerable to epigenetic errors. This occurs
soon after fertilization, near the time of blastocyst and Inner Cell Mass
(ICM) formation (Santos et al. 2002; Dodge et al. 2004; Surani and Reik
2007; Denomme and Mann 2012). Although both DNA methylation and
numerous histone modi
cations are known to be involved in epigenetic
programming, most evidence is now restricted to the less complex
pattern of DNA methylation. Rapidly after fertilization the male genome
is actively demethylated. Depending on species, the female genome is
passively demethylated usually between the 4 and 64 cell stages. The
epimarks of DNA methylation are replaced
de novo
to help establish the
pluripotent programs at the blastocyst ICM stage. Here methyl epimark
errors are most likely to occur. Mouse ICM cells can be cultured in
