I find this lecture really informing. I have one from of intersex. During gestation my germ cells failed to fully reach the gonads. Thus one gonad remained as a fetal gonad, ovotestis and an attached germ cell teratoma. Depending on how you define it. My other gonad did develop as a testis but remain small and immature. If that were not enough I have a number of germ cell teratoma found in various areas of my abdomen. Two were removed when I was ten years old and several others were found when I was an adult. These teratoma were 10 cm and 17.5 cm when surgically remove. The 10 cm one happened to also be malignant. I tend to be asexual but also see myself as being transgender.
expected to learn more on Mary Lyon's experiments that led her to this groundbreaking conclusion, someone please let me know any source to learn about that!
Great lecture . I always maintained that junk DNA is a false statement of incomplete scientific knowledge. Of interest is if increase in gene expression requires a fine tuning expression , in other words is overexpression of a particular gene beneficial and chronologically determinant.
Im confused about this the use of the term "choice" in allelic choice in x-nactivation as its random X-inactivation. Do you just mean how one is inactivated and other one not?
fascinatiing. When you say that this is something that all mammals do, am i correct in assuming that this does not happen in non mammals, for example, reptiles? if so, why?
Hello, how could we say in the X-linked inheritance that there is a carrier or pure form if the second x chromosome is inactivated anyway and how the presence of one x chromosome would affect if always the only one X is activated.
Hmmmm. If inactivation turns us basically into Turners, why do Turners have a recognizable condition? Or they turn off that one by mistake in some cells?
Females can still be affected by X linked diseases but it’s a little more tricky than it seems. If it’s a dominant condition and the affected X is active, the disease will be present; if it’s a recessive condition (only presents in homozygous) then the other unaffected X can compensate for it, and if it’s the unaffected X that’s active the disease will not be present.
I had the same question, particularly with regard to color-blindness, which, as I understand it, is a X-linked recessive condition. The best explanation that I could come up with in view of what was presented in this lecture, was in terms of the random “mosaic” of activation in the cells of a female. So consider a female having two X-chromosomes, one of which carries the allele for colorblindness and the other carries the normal allele. Because the cells in the female will be a “mosaic” composed of cells in which either one of the X-chromosomes is inactive, about half the cells will have the X-chromosome with the normal allele as the active one, staving off color-blindness (and similarly other X-chromsome linked recessive conditions). Fascinating lecture, but as in much of Biology, generated more questions than it answered!
Must say... Dr. Lee is an incredible lecturer. Well outlined and fluid presentation. The graphics were superb as well!
A super lecture, very well presented. Thanks Jeannie Lee and iBiology!
This channel is amazing
Absolutely
I find this lecture really informing. I have one from of intersex. During gestation my germ cells failed to fully reach the gonads. Thus one gonad remained as a fetal gonad, ovotestis and an attached germ cell teratoma. Depending on how you define it.
My other gonad did develop as a testis but remain small and immature.
If that were not enough I have a number of germ cell teratoma found in various areas of my abdomen. Two were removed when I was ten years old and several others were found when I was an adult. These teratoma were 10 cm and 17.5 cm when surgically remove. The 10 cm one happened to also be malignant.
I tend to be asexual but also see myself as being transgender.
@Ismael barrera Interesting! I’ll have to digest this information and do more study
expected to learn more on Mary Lyon's experiments that led her to this groundbreaking conclusion, someone please let me know any source to learn about that!
With the references too
Great lecture . I always maintained that junk DNA is a false statement of incomplete scientific knowledge. Of interest is if increase in gene expression requires a fine tuning expression , in other words is overexpression of a particular gene beneficial and chronologically determinant.
What an amazing lecture!!
Im confused about this the use of the term "choice" in allelic choice in x-nactivation as its random X-inactivation. Do you just mean how one is inactivated and other one not?
fascinatiing. When you say that this is something that all mammals do, am i correct in assuming that this does not happen in non mammals, for example, reptiles? if so, why?
Hello, how could we say in the X-linked inheritance that there is a carrier or pure form if the second x chromosome is inactivated anyway and how the presence of one x chromosome would affect if always the only one X is activated.
If you reactive the inactive X, will it also inactive the previously active X? otherwise wouldn’t it lead imbalance and cause other problems?
Hello mam
My question is, the inactivation of x chromosome have any effect on autosomal genes?
thank you
Hmmmm. If inactivation turns us basically into Turners, why do Turners have a recognizable condition? Or they turn off that one by mistake in some cells?
Because there’s control mechanisms, the inactivated X is not turned useless, it is still used to control/balance the active X
severe phenotype character are seen in turners due to deficiency in escape genes from silencing.
Not all genes are silenced on the inactive X. A bunch of genes escape inactivation.
It’s not all inactive still 10% xicst rna but which one gets inactived israndom and it happens in mammals for dosage compensation
Does anyone know which x passes down to germ cell during meiosis in females and how this process is reversed
Very nice
Then how are females safe from X linked or sexlinked diseases if this phenomenon occurs?
What happens then?
Females can still be affected by X linked diseases but it’s a little more tricky than it seems. If it’s a dominant condition and the affected X is active, the disease will be present; if it’s a recessive condition (only presents in homozygous) then the other unaffected X can compensate for it, and if it’s the unaffected X that’s active the disease will not be present.
@@bearpancakes so in a recessive condition if the unaffected X is silenced then the disease will be present, yea?
I had the same question, particularly with regard to color-blindness, which, as I understand it, is a X-linked recessive condition. The best explanation that I could come up with in view of what was presented in this lecture, was in terms of the random “mosaic” of activation in the cells of a female. So consider a female having two X-chromosomes, one of which carries the allele for colorblindness and the other carries the normal allele. Because the cells in the female will be a “mosaic” composed of cells in which either one of the X-chromosomes is inactive, about half the cells will have the X-chromosome with the normal allele as the active one, staving off color-blindness (and similarly other X-chromsome linked recessive conditions). Fascinating lecture, but as in much of Biology, generated more questions than it answered!
My name is Jeannie
What about intersex?
Which definition are you talking about?
"there are no supernumerary Xes" - with some excepions ;)
That why you not advanced in genitc and u will never be until understanding the polarities of these jens
First it's not y x. It's h and small x for what we gain from eating that is important to live your so wrong and I proud to tell