1a.) meiosis, the ovary must produce germ

1a.)      Meiotic prophase occurs within the fetal
ovary and involves synapsis and recombination. Approximately 12 weeks after
fertilization, meiosis will begin in the fetal ovary. Oocytes will first enter
prophase where the nuclear envelope breaks down and homologous chromosome
pairing occurs (“The Process of Meiosis”, n.d.). This pairing of homologous
chromosomes is referred to as synapsis. After homologous chromosomes have been
paired together, the synaptonemal complex is formed and allows for genetic
information to be transferred between the non-sister chromatids. This process is
called recombination and results in increased genetic variation. After recombination,
the cell is in the diplotene stage of prophase. During the diplotene stage of
prophase, the oocyte enters dictyate, a prolonged state of arrest (Hunt &
Hassold, 2008).

1b.)      Synapsis and recombination events that
occur during prophase in early fetal development can contribute to aneuploidy
later in life (Williams, 2018). Synapsis and recombination are therefore critical
in determining the potential for segregation errors in the future. Hunt and
Hassold (2008) also suggests that errors in the exchange of genetic material
can result in a significant decrease in meiocytes.

1c.)      It has long been known that genetic factors
can be responsible for errors in synapsis and recombination. However, recent
research has suggested that environmental factors can also result in changes in
recombination patterns (Hunt & Hassold, 2008).  For example, Bisphenol A or BPA is a common
food contaminant and can result in increased errors in synapsis in the fetal
ovary as well as increased errors in the placement of recombination. These errors
can then transfer to errors during anaphase and result in chromosome
abnormalities. Rodents exposed to BPA showed increased reproductive detriments,
early onset puberty and decreased sperm levels (Hunt & Hassold, 2008).

2.)        Hunt and Hassold (2008) suggests that the
packaging of oocytes into follicles can be influenced by environmental factors along
with genetic factors. Before the follicle can undergo meiosis, the ovary must
produce germ cell cysts through the mitotic proliferation. Before a follicle can
form, an individual cell must be captured by granulosa cells. Exposure to certain
environmental factors can alter the formation of the follicle and can lead to a
single follicle that contains more than one oocyte. Multioocyte follicles can have
a detrimental impact on reproductive health involving decreased in reproductive
lifespan and poor-quality oocytes.

3a.)      As discussed earlier, meiotic prophase
involves pairing of homologous chromosomes called synapsis and exchange of genetic
material called recombination. In order for the homologous chromosomes to
tightly pair, there must be connections called chiasmata. Cohesin proteins are used
to hold sister chromatids together until they are separated in anaphase of
meiosis 2 (“The Process of Meiosis”, n.d.). Since the chiasmata were made
during prophase of fetal development, the proteins used to hold the chiasmata
are thought to have been just as old as the chromosomal connections themselves.
Authors Hunt and Hassold (2008) therefore conclude that a 45-year-old woman
must be reliant on these same cohesion proteins to keep homologs together and
in dictyate arrest.

3b.)      Mice exposed to BPA during oocyte growth
resulted in differences in the alignment of chromosomes along the metaphase plate
as well as increased incidence of non-disjunction events.

4.)        Research conducted by Kong et al. set
out to estimate the number of new mutations found in an offspring’s DNA. Kong
et al. (2012) estimated that a total of 60 new mutations are passed on with
each generation. After sampling mother, father and offspring, it was found that
mutations inherited from the mother were constant at around 15 mutations per
generation. However, mutations from the father ranged from 25 to 65 mutations,
depending on age (Kondrashov, 2012). Findings suggest that younger fathers
produce offspring with less single point mutations than fathers of increased age.
An increase in single mutations can accumulate and then result in increased incidence
of genetic disorders. Research conducted by Kong et al. therefore aimed at
determining the effects of paternal age on the incidence of genetic disorders.

5.)        De novo mutations increase with paternal
age, but not maternal age. This is because female germ cells, or oocytes are not
undergoing constant state of division. Sperm cells however, are constantly
dividing, leaving more opportunity for errors with the increased number of cell
divisions. This means that accumulation of errors can be more detrimental in older
fathers and therefore lead to increased number of mutations transmitted to the
next generation.

6.)        The Hughes articles discusses a different
mechanism of inheritance, epigenetic inheritance. This mode of inheritance looks
at how different environment exposure of parents can affect their offspring. Essentially,
environmental assaults leading to adverse health affects in parental generations
can be inherited by their offspring.

7.)        The Hughes articles only focusses on
paternal effects for epigenetic inheritance. This is because it can be
difficult to distinguish the differences between maternal epigenetic inheritance
with environmental exposures during pregnancy (Hughes, 2014). Since men cannot
influence the fetus after fertilization, any potential epigenetic inheritance
cannot be attributed to other factors.

8.)        Dias and Ressler (2014) exposed mice to
a sweet chemical compound called acetophenone along with an electrical shock. This
allowed the mice to attribute the sweet smell to a fear shock. Anytime the mice
were exposed to acetophenone, they became anxious and fearful (Hughes, 2014).
Dias and Ressler then mated the treated mice with untreated females. When the
resulting offspring were exposed to acetophenone, they reacted in a similar
manner as their fathers. Even after 2 generations, mice became afraid after acetophenone
exposure. Dias and Ressler (2014) concluded that the similar sensitivity to
acetophenone occurred due to epigenetic inheritance. It is hypothesized that
changes in the parental genome occurred, altering the representation of DNA,
whilst maintaining the sequence of the DNA. This modification to the expression
of DNA was then inherited by the offspring (Hughes, 2014).

9.)        Scientists are still unsure about how
epigenetic inheritance occurs. In order for epigenetic information to be
inherited, it must avoid several intense rounds of epigenetic reprogramming or
scrubbing. This involves removing all epigenetic markers during processes of
demethylation, and re-methylation during embryonic development. Scientists are
unsure about how certain traits can escape or be unaffected by this process of
reprogramming.