The manifestation of the Sexual Dimorphism Personality Spectrum Tapestry is a result of the influence of ALL of the Filters, Ensembles, and Tapestries related to human perception, response, and behavior.

Sexual Dimorphism is instinctive within the Cognitive Me. "It is not taught. It is there."

Therefore a listing of the various other filters that impact the manifestation of the Resilience Personality Spectrum Tapestry would in fact list ALL OF THEM.

We will list a few.

All of the Personality Filters are in play when it comes to wanting to fully understand Sexual Dimorphism, because they are all in play when wanting to fully understand The Me.

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The Sexual Personality Dimorphism Spectrum Tapestry

Let's look at some of the various (normal and alternate) mammalian sexual chromosome environments that impact other traits that arise from the non-sexual autosomal chromosome domain. The XY sex-determination system.

Recall that as eukaryotes, our somatic cells are diploid. One haploid copy is contributed by the mother, and the other haploid copy is contributed by the father. The chromosomes are all packaged together in the cellular nucleus. Each of the autosomes is paired with its corresponding autosomal partner ... chromosome 1 with 1, 2 with 2, etc.

The allosomes (the X and Y chromosomes in mammals) are an exception to the rule of 1 with 1, 2 with 2, etc. The X and the Y chromosomes (allosomes) differ from each other and yet may be paired with each other (normally as either XX or XY). When two X's pair with each other (one from the father, the other from the mother) the result is a female. When an X and a Y pair with each other the result is a male.

It turns out that the X:Y ratio is a significant determinant with regard to how eukaryotes develop physically. The genes present on these allosomes are different. Thus, an XX (a genetic female) has twice the X gene dosage of an XY (a genetic male), and it has none of the Y genes. The XY has only half the X gene dosage that an XX has, and it has the Y genes that an XX does not have. Ultimately, all hereditary physical and behavioral traits are gene based. Thus, XX and XY individuals of the same species will manifest differing physical and behavioral attributes.

The Dimorphism Spectrum Tapestry, which we all have manifested with one another. From this, The Sexual Dimorphism Spectrum Tapestry, which describes the various differences between the male and female demographics that comprise our species. A subset of this is The Sexual Personality Dimorphism Spectrum Tapestry.

An understanding of the Asymmetry of the Filters suggests that to even get close to being able to understand another empathetically ("Do I know what it may be like to be You in Your shoes?") one needs to be expressing the same filters and most of them at very similar dial settings. Perfect matches are impossible (a Fundamental Prerequisite) but we often get close enough. However, achieving "close enough" filter matches between XX and XY individuals is completely impossible due to the gene dosage issues and the way that differing X:Y ratios impact physical, cognitive, and experiencial filter development.

We may be able to get along. But we will not truly "get" each other. Close enough is not "getting each other." How close is "close enough" anyway?

Stereotypical asymmetric "getting it" is often observed. Most guys "get" most guys and most "gals" get most "gals". Yet the males often think they get the females ... but generally don't. And the females often think they get the males ... but generally don't. This leads to communication differences depending on the gender one is communicating with, giving rise to the notion of quad-dimensional (i.e. XX to XX, XY to XY, XX to XY, and XY to XX) entendres!

While rare, various divergences from genetic "normalcy" occur throughout all species. Let's examine the more commonly seen X:Y ratio types.

• XX
  • condition 1 - results in normal female
    
    
  • condition 2 (intersex) - XX male syndrome - a rare syndrome diagnosed in 1:20,000 males, 90% of the time the result of unequal crossing over between the X and the Y in the male during meiosis prior to gametogenesis (spermatogenesis.) In XX male syndrome, this crossover "error" has usually resulted in the SRY gene being relocated to the X rather than the Y. The X contributed by the father now comes with the SRY gene rather than on the Y where it is normally found. Thus, an individual with a female (XX) genotype has phenotypically male characteristics.
  
  
• XY
  • condition 1 - results in normal male
    
    
  • 
    Hanne Gaby Odiele. XY male genotype
    w/ androgen insensitivity syndrome (AIS).
    Hanna tells her story.
    condition 2 (intersex) - Androgen insensitivity syndrome (AIS). Prevents or impairs the masculinization of male genitalia in the developing genetic male (XY) fetus, as well as the development of male secondary sexual characteristics at puberty.
    
    The androgen receptor (AR) gene (NR4C4) is located on the X chromosome. In the case of AIS, the AR is unresponsive to testosterone. The way a normal AR works is that when exposed to testosterone, it binds to it, then translocates to the nucleus, where it binds to DNA when other cofactors are present. This complex then activates gene expression. These genes are thus androgen responsive. However, they aren't if the AR is defective, and doesn't bind testosterone or translocate!
    
    Of course, there is not simply one way that this regulatory system can become defective. There are many ways. Think about it.
    
    
    
    Phoebe Hart. XY male genotype
    w/ androgen insensitivity syndrome (AIS).
    Interestingly, since the AR gene is located on the X, and since normal females are XX, then normal females can carry both a defective and a working AR gene and remain healthy. They have a 50% chance of passing the defective AR gene on to a male child. When that happens, AIS occurs. The genes that are regulated by the testosterone bound AR complex are found on several chromosomes.
  
  
• True hermaphrodite - Pregnancy in a hermaphrodite with a male-predominant mosaic karyotype
  
  
• X0 - Turner syndrome. Due to a chromosomal abnormality in which all or part of one of the X chromosomes is missing or altered. Signs and symptoms vary. Often, a short and webbed neck, low-set ears, low hairline at the back of the neck, short stature, and swollen hands and feet are seen. They typically develop menstrual periods and breasts only with hormone treatment, and are unable to have children without medical intervention. Heart defects, diabetes, and low thyroid hormone occur more frequently. Most have normal intelligence. Many have troubles with spatial visualization that may be needed for mathematics. Vision and hearing problems occur more often.
  
  
• XXY - Klinefelter syndrome. Primary features are sterility and small testicles. Often, symptoms may be subtle. Sometimes, symptoms are more prominent and may include weaker muscles, greater height, poor coordination, less body hair, breast growth, and less interest in sex. Intelligence is usually normal. Reading difficulties and problems with speech are more common. Symptoms are typically more severe if three or more X chromosomes are present (XXXY syndrome or 49,XXXXY). XXY males are also more likely than other men to have certain health problems that typically affect females, such as autoimmune disorders, breast cancer, venous thromboembolic disease, and osteoporosis.
  
  
• XYY - XYY syndrome. Symptoms are usually few. They may include being taller than average, acne, and an increased risk of learning problems. The person is generally otherwise normal, including normal fertility. People with the 47,XYY karyotype have an increased growth velocity from early childhood, with an average final height approximately 7 cm (3") above expected final height.
  
  
• XXYY - XXYY syndrome. Recall that the appearance of at least one Y chromosome with a properly functioning SRY gene makes a male. Therefore, humans with XXYY are genotypically male. Males with XXYY syndrome have 48 chromosomes instead of the typical 46. Extra copies of genes on the X chromosome interfere with male sexual development, preventing the testes from functioning normally and reducing the levels of testosterone. Many genes are found only on the X or Y chromosome, but genes in areas known as the pseudoautosomal regions are present on both sex chromosomes. Extra copies of genes from the pseudoautosomal regions of the extra X and Y chromosome contribute to the signs and symptoms of 48,XXYY syndrome.
  
  Among the impacts: developmental delays, speech impairment, behavior outburst and mood swings, intellectual impairment, autism spectrum disorders, tall stature, scoliosis, clinodactyly, low muscle tone, sterility, delayed sexual development, undescended testes.
  
  
• XXX - Triple X syndrome
  
  
• XXXX - Tetrasomy X
  
  
• XXXXX - Pentasomy X

A detailed listing of the genes, their products, and the systems in play that result in the manifestation of male and female behavioral, perceptual, instinctual, and physiological characteristics is beyond the scope of this chapter. It is also not possible given our current knowledge.

However, one example will be given, picked at random, as a peek at the complexity that is beginning to be understood regarding the genesis of sexual dimorphism. Not surprizingly, what is known does not differ in the abstract from what is known about other biological systems, their development, their regulation, and their response to the environment they find themselves within. The details differ. The complexity, although astounding, does not.

The following example does not involve the AR gene, but does involve a gene that produces a protien that interacts with AR, among other systems.

Structure of the NR5A1 protein.

Steroidogenic factor 1 (SF-1) protein is a transcription factor involved in sex determination by controlling activity of genes related to the reproductive glands or gonads and adrenal glands. Other roles in endocrine function have been discovered. This protein is encoded by the NR5A1 gene, a member of the nuclear receptor subfamily, located on the long arm of chromosome 9 at position 33.3.

Following sequence specific DNA binding, trans-activation of target genes depends on recruitment of co-activators such as SRC-1, GRIP1 (note, possible glutamate neurological receptor involvement in learning and memory), PNRC (note, a coactivator of several other nuclear receptors), or GCN5. The hinge region can undergo post-transcriptional and translational modifications that further enhance stability and transcriptional activity.

In males, SF-1 (NR5A1) transcripts precede the onset of SRY (sex-determining region Y protein) expression in the fetal testes hinting at gonadal developmental role. SRY influences the differentiation of the fetal testes into distinct compartments: testicular cords and interstitial region containing Leydig cells. Increase in SF-1 protein and detection in the steroidogenic Leydig cells and testicular cords coincides with development.

However, in females, in the ovaries, gonadal sexual differentiation is facilitated by reductions in SF-1 transcript and protein. SF-1 levels are strongly expressed at the onset of follicular development in theca and granulosa cells which precedes expression of the aromatase enzyme responsible for estrogen biosynthesis.

Other genes related to sexual dimorphism development are included in the Multfilters subsection of this section.

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A Few Systems Examples that contribute to the manifestation of Sexual Dimorphism:

• Multiple Filters In Play for The Libido Personality Spectrum Tapestry. Yea, that's a big one that significantly influences what and who "The Me" manifests as "me."
  
  
  
  Papaver somniferum flower
• Multiple Filters In Play for the Humor Personality Spectrum Ensemble.
  • Discussion of the mesolimbic dopamine pathway and the Reward System.
    
    
  • The opioid system, naturally, is mentioned as well. Consider the instinctive Resilience of the Cognitive Me and its draw to Home. Home is where resonance (harmony) is. Consider that the feeling of "being home" tends toward the euphoric.
    
    The body makes morphine endogenously, for its own use. Morphine is among the MOST euphoric drugs known.
    
    
• The Environment. All of "What We Are" is influenced to some degree by the environments we find ourselves needing to survive within.
  
  
• The androgen receptor (AR) gene (NR4C4) is located on the X chromosome. In the case of AIS, the AR is unresponsive to testosterone. The way a normal AR works is that when exposed to testosterone, it binds to it, then translocates to the nucleus, where it binds to DNA when other cofactors are present. This complex then activates gene expression. These genes are thus androgen responsive. However, they aren't if the AR is defective, and doesn't bind testosterone or translocate!
  
  Steroidogenic factor 1 (SF-1) protein is a transcription factor involved in sex determination by controlling activity of genes related to the reproductive glands or gonads and adrenal glands. Other roles in endocrine function have been discovered. This protein is encoded by the NR5A1 gene, a member of the nuclear receptor subfamily, located on the long arm of chromosome 9 at position 33.3.
  
  Following sequence specific DNA binding, trans-activation of target genes depends on recruitment of co-activators such as SRC-1, GRIP1 (note, possible glutamate neurological receptor involvement in learning and memory), PNRC (note, a coactivator of several other nuclear receptors), or GCN5. The hinge region can undergo post-transcriptional and translational modifications that further enhance stability and transcriptional activity.
  
  In males, SF-1 (NR5A1) transcripts precede the onset of SRY (sex-determining region Y protein) expression in the fetal testes hinting at gonadal developmental role. SRY influences the differentiation of the fetal testes into distinct compartments: testicular cords and interstitial region containing Leydig cells. Increase in SF-1 protein and detection in the steroidogenic Leydig cells and testicular cords coincides with development.
  
  However, in females, in the ovaries, gonadal sexual differentiation is facilitated by reductions in SF-1 transcript and protein. SF-1 levels are strongly expressed at the onset of follicular development in theca and granulosa cells which precedes expression of the aromatase enzyme responsible for estrogen biosynthesis.
  
  
• Other genes related to sexual dimorphism (development either as male or female):
  • SOX-9 - Acts during chondrocyte differentiation and, with steroidogenic factor 1, regulates transcription of the anti-Müllerian hormone (AMH) gene. Note, in the absence of SOX-9 and SRY, no testes can develop and the path is clear for the development of ovaries. SOX-9 is located on chromosome 17q24.
    
    
  • Forkhead box protein L2 (FOXL2). FoxL2 is a marker for ovarian differentiation, and is required for granulosa cell differentiation. In addition, the foxl2 protein will prevent the formation of testes by suppressing expression of SOX9.
    
    
  • Doublesex and mab-3 related transcription factor 1 (DMRT1). gene.
    
    
  • There are several genes present on the Y which do not have homologs on the X chromosome. In addition, there are homologs on the Y that are also present on the X and are believed to have gotten there via X/Y translocation events thousands and millions of years ago. For example:
    
    
    • Protocadherin 11Y (PCDHY) - is a gene unique to human males and is located on the Y chromosome. It encodes Protocadherin 11Y, a protein that guides the development of nerve cells. It, and its homolog, PCDH11X (located on the X chromosome), is thought to play a fundamental role in cell-cell recognition essential for the segmental development and function of the central nervous system.
      
      PCDH11X and PCDH11Y respond in different ways to Retinoic acid, a chemical involved in the development of embryos. The acid stimulates the activity of PCDH11Y but suppresses PCDH11X. This is likely one of the explanations for the differences between the brains of men and women.
      
      To delve a little further, retinoic acid, during early embryonic development, helps determine position along the embryonic anterior/posterior axis by serving as an intercellular signaling molecule that guides development of the posterior portion of the embryo. It acts through Hox genes, which ultimately control anterior/posterior patterning in early developmental stages.
      
      Humans have 38 Hox genes. Picking one randomly, Homeobox protein Hox-A1 (HOXA1) may be involved in the placement of hindbrain segments in the proper location along the anterior-posterior axis during development. A common polymorphism in the HOXA1 gene is associated with a susceptibility to autism spectrum disorder. Homeobox protein Hox-A11 (HOXA11) is involved in the regulation of uterine development and is required for female fertility.
  
  
• Fetal Development: Your Baby's Sex - A factually based description of fetal sexual development that is approachable by the lay audience.
  
  
• Endotext.org, Sexual Differentiation, June 2016 - Very Important Chapter
  
  Numerous hormones and growth factors are involved in sex determination and differentiation. Both an active genetic pathway towards ovarian development and female gonadal differentiation as well as hormone related pathways determining testicular development and differentiation of the male reproductive tract are discussed.
  
  Several genes located both on the sex chromosomes (allosomes) and the autosomes involved in sexual differentiation and dimorphism are discussed.
  
  
• Embryology, BGDB Sexual Differentiation - An introduction to the earliest events in Sexual Differentiation.
  
  

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Each of these "Sexual Dimorphism Personality Ensembles", which altogether make up the Sexual Dimorphism Spectrum Tapestry, are themselves tapestries and ensembles of Filters or other Ensembles (such as the Humor Ensemble.)

While the Sexual Dimorphism Ensemble's activity may be independent of environmental influence (it is instinctual only, and is either active within a default phenotypic manifestation range or it is not), multiple things fall out of the fact that how it manifests itself responds to the Environment (it is adaptable):

• It will be difficult to uncover many of the biological components that create the Dimorphism Spectrum Tapestry, including its subset component - the Sexual Dimorphism Tapestry. There are many hundreds, at least.
  
  
• Different environments impact one's adaptive manifestation of the Dimorphism Spectrum Tapestry status. Uncovering and describing the full mechanism of action (MOA) resulting in the manifestation of this tapestry, unique to each one of us, will be both confounding and fascinating.
  

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