BIOL10210 Lecture Notes - Lecture 12: True Hermaphroditism, Pseudohermaphroditism, Xyy Syndrome

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25 Apr 2018

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Intersexuals and hermaphrodites: (cid:1005) i(cid:374) (cid:1005)(cid:1004)(cid:1004) (cid:271)irths is (cid:374)ot (cid:862)(cid:374)or(cid:373)al(cid:863) (cid:373)ale or fe(cid:373)ale, genitalia may be ambiguous or both genitalia may be present. X0: also infertile, iq usually normal, 1/2500 female births. Above average numbers of violent criminals have this condition. Hermaphroditism is a special type of intersexual condition in which an individual is born with both ovarian and testicular tissue. No documented case of true hermaphroditism in humans, only pseudohermaphroditism. One or the other genitalia, or both are sterile. When it comes to other animals aside from humans, we have already talked a little bit about sequential hermaphrodites. In the rest of the animal kingdom, 24 or 34 phyla are known to have hermaphrodites. In some cases it is the most common sexual form. In a very few cases the individuals can self-fertilize. Ba(cid:271)y appears fe(cid:373)ale a(cid:374)d is raised fe(cid:373)ale, (cid:271)ut is 46 xy. Baby appears female and is raised female but is 46.

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Kindly write a one page summary of the data below.

A crucial assumption underlying most models of sexual selection is that sexual advertisements honestly reflect the phenotypic and/or genetic quality of their bearers (1). Here we show that experimental activation of the immune system is rapidly mirrored in the expression of a carotenoid-based secondary sexual trait in male blackbirds (Turdus merula). This result shows that sexual advertisement honestly signals male health and can be reliably used by conspecifics as a cue of individual quality during intra- and/or intersexual interactions. Male blackbirds exhibit a black plumage with a yellow to orange bill, whereas females are brownish with a brown bill. Recent studies have suggested that bill color is a sexually selected trait in blackbirds (2, 3). For example, resident male blackbirds are more aggressive to mounts with orange bills than to mounts with yellow bills (2). Bill pigmentation might therefore provide a signal used during contests between males (2). In addition, male blackbirds with orange bills are mated with females in better body condition and fledge more offspring than males with yellow bills (3). Overall, these results suggest a role for bill color in sexual selection, possibly as an indicator of male phenotypic quality. Carotenoids are common components of colored signals used in animal communication (4). They are also important in the up-regulation of various aspects of the immune functioning (5) and cellular protection against free radicals (6). This suggests that a trade-off may exist between allocation of carotenoids to sexual signaling versus immune defenses (4). Using an autosampler high-performance liquid chromatographer, we determined the presence of carotenoids deposited in the bill of male blackbirds [see note (S1)] (7). The analysis of the absorption spectrum revealed the presence of - and -carotene, -cryptoxanthin, zeaxanthin, and lutein (Fig. 1A). To investigate whether bill color reflects immune status, we immunized captive male blackbirds with a suspension of sheep red blood cells (SRBC) in both spring 1999 (n 19) and spring 2002 (n 13). A control group (n 15) was injected with a phosphate-buffered saline solution (PBS) for control in 2002. Only the 2002 birds were used as a direct test of the hypothesis that immune activation reduces the expression of the secondary sexual trait, by comparing changes in bill color for SRBC and PBS males. Birds immunized with SRBC in both years (n 32) were used to assess the effect of anti-SRBC immune response on bill color [see note (S2)] (7). The humoral immune response against SRBC was determined 7 days after the challenge with a haemagglutination technique. Birds immunized with SRBC displayed a significant decrease in bill color [repeated measurements analysis of variance, F(1,26) 14.34, P 0.0008; Fig. 1, B, C, and D], which was independent of initial bill color and was not associated with a decrease in body mass (P 0.1). In addition, among immunized males, the likelihood of becoming duller was significantly correlated with the intensity of the anti-SRBC response as determined from the haemagglutination test (logistic regression, Wald 2 5.12, P 0.023, n 32), whereas neither year nor initial bill color entered the logistic regression model (P 0.1). Overall, these results demonstrate the existence of a trade-off between sexual advertisement and immune activation in male blackbirds. This finding has important consequences for both the evolution of secondary sexual traits and the cost of immune function. Assessment of opponent quality during male-male competition or mate quality during female choice based on a dynamic trait, such as bill color, might have evolved if it honestly reflects health status of the individual (1). The activation of the immune system by an infectious process is rapidly mirrored in the color of the bill. Contrary to feather ornaments that are produced during the annual molt, dynamic traits might therefore convey a continual update on male health. Carotenoids, such as astaxanthin, lutein, and -carotene, used for sexual signaling have been shown to enhance in vitro and in vivo antibody production to SRBC (8) and to provide protection against free radicals (6). Our results suggest that the activation of the immune system withdraws carotenoids to enhance immune functioning as well as to deal with free radicals produced during the immune response, at the expense of sexual signaling.

aquamarinewallaby935

A male patient age 15 comes into your clinic presenting the symptoms of mental retardation, behavioral abnormalities, including hand flapping and hyperactivity. Additionally, you notice this patient has some facial abnormalities, including large ears and a prominent jaw and forehead. Due to the mental retardation, you initially suspect that this disorder may be a trisomy of chromosome 21.

1. (2 points) Is trisomy 21 a chromosomal or single gene disorder? Please explain why.

2. (3 points) Please describe an experimental technique you could use to determine whether the patient has trisomy 21. Include in your description, what the experimental result would be if he did have trisomy 21, or he did not?

After performing the technique you described in question 2, you find out that he did not have the trisomy 21. You next ask the family if there are other members afflicted with the disorder and the answer is yes. Afterward, you get a full family history and put it together to form a pedigree.

After realizing that this is a single gene disorder, you believe the patient is suffering from Fragile X Syndrome. Answer the following questions below based on Fragile X syndrome.

4. (1 point) What gene is affected in Fragile X syndrome?

5. (1 point) Please create a list of symptoms a Fragile X patient may have?

6. (2 points) Based on the symptoms above, please discuss briefly why you may have been initially tricked into thinking this disorder was a chromosomal disorder.

7. (1 point) Please go to page 262 in your book, and explain in detail the nature of the mutation that causes Fragile X syndrome.

8. (2 points) Of the two techniques listed below, which would best allow you to state whether the patient has Fragile X syndrome? Please explain your answer.

a. PCR

b. RFLP

9. (2 points) Please answer question 9 using the information from questions 7 and 8. You analyze your data from the PCR reaction from question 8, which amplifies the region were the insertion lies. You notice that the patientâs sister has a single band on the gel at 45 base pairs. You notice the mother has a band at 200 base pairs and a band at 45 base pairs. The patient has a single band on the gel at 200 base pairs, and the father has a single band at 45 base pairs.

a. What is the genotype of the father and what is the phenotype of the sister?

b. Based on the experiment, what is the size of the insertion region in the wild-type allele, and what is the size of the insertion region in the mutant allele?

c. What is the actual size of the insertion (Hint: think about the difference in the sizes of the insertion region)

I'll be thankful if someone can help me to do this!

According to this:

Read the following New York Times article and then answer the questions below and then answer the questions New Clues to Sex Anomalies in How Y Chromosomes Are Copied

http://www.nytimes.com/2009/09/15/science/15chrom.html?scp=1&sq=sex%20anomalies&st=cse

This activity contains 5 questions.

When discarding bad genes, what does the Y chromosome recombine with?

	the other Y chromosome
	the compliment X chromosome
	itself
	nothing

What holds a pair of copied chromosomes together?

	chromatid
	centrosome
	centromere
	chromatin

A person with Turner's syndrome has which of the following?

	a single X chromosome
	two X chromosomes
	a single Y chromosome
	two Y chromosomes

Where is the male-determining gene on the Y chromosome?

	close to the end of the right arm
	close to the end of the left arm
	near the middle of the right arm
	near the middle of the left arm

Briefly explain how an individual can have some cells with no Y chromosome and other cells with a double-Y chromosome . (in your response, go beyond the article, search the web, use experiences from your life, broaden your horizons)

You must make 2 reflective, thoughtful, deep, constructive critiques of your class mates posts. as part of a threaded discussion following their initial post. The critiques must not about you, but about science!

Here's the first peson. Needs to reply for some of her answers as it says above.

1. When discarding bad genes, the Y chromosomes recombines with itself.

2. The centromere functions to hold a pair of copied chromosomes together.

3. A person with Turnerâs syndrome is born with a single X chromosome.

4. The male-determining gene on the Y chromosome is located close to the end of the left arm.

5. An individual can have some cells with no Y chromosomes and other cells with double Y chromosomes, due to the differing variants present in regards to the genotypes of the cells in a single individual. When the Y chromosome is compared to other chromosomes such as the X chromosome, mutations and deviation in the distance of the centromere are much more prevalent due to the Y chromosome lacking a backup system to promote repairs.¹ (Links to an external site.) Even if a mutation caused a condition such as the XYY syndrome where two Y chromosomes are present, that mutation and genotype would not be present in every single cell of the individual.² (Links to an external site.) The presence of different genotypes offers an tentative explanation to as why a single individual can have some cells with no Y chromosomes while also housing other cells with double Y chromosomes.

Source 1 http://www.nytimes.com/2009/09/15/science/15chrom.html

Source 2 https://www.healthline.com/health/xyy-syndrome

Here's the second person. Needs to do the same as it says above.

1. Itself

2. Centromere

3. A single X chromosome

4. Close to the end of the left arm

5. Briefly explain how an individual can have some cells with no Y chromosome and other cells with a double-Y chromosome.

In some cases, the Y chromosome reaches over to a neighboring counterpart and the two chromosomes fuse. This results in the loss of part of the chromosome. Jacobâs Syndrome is sometimes also called XYY syndrome because the person has two Y chromosomes. Although a person can survive with this genetic mutation, some physical traits may be observed such as taller than average height, weak muscle development or late speech development.

Source 1 https://www.healthline.com/health/xyy-syndrome

Source 2 http://www.isna.org/faq/y_chromosome

BIOL10210 Lecture Notes - Lecture 12: True Hermaphroditism, Pseudohermaphroditism, Xyy Syndrome

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