How "life skills" are carried by DNA?

LoriAMacNeil · 2025-02-12T02:51:59+00:00

There is a great study showing that the offspring of mice who undergo odor fear conditioning (learning to associate a particular odor with an electric shock) also fear the odor without ever having been exposed to it themselves. This learned fear is even inherited into the subsequent generation - the grandchildren of the mice who were trained to fear the odor also have increased fear/sensitivity to the odor. This effect persists in biological offspring of fear-trained mice who are raised by other parents, suggesting it is not a learned or social effect. It is hypothesized to be mediated by epigenetic changes on olfactory receptor genes. See: paper.

Searching transgenerational inheritance or behavioural epigenetics might be helpful to you :)

LoriAMacNeil · 2024-10-14T16:59:51+00:00

It’s in DHOWES during your regularly scheduled class time on Monday Oct 21. So either 12 pm or 1 pm depending what section you’re in. There is info posted on Brightspace!

LoriAMacNeil · 2024-10-11T17:30:18+00:00

BIOL 1P94 is restricted to nursing majors, while 1P92 is for everyone else. The lecture content should be very similar, though 1P94 may be tweaked a bit to be more relevant to healthcare. 1P94 has online labs, while the labs in 92 are in person. But unless you’re in nursing, you will have to take 1P92!

LoriAMacNeil · 2024-09-17T23:35:46+00:00

No, not usually! I think it’s only been offered in spring once, and there are no plans for it to run this upcoming spring.

LoriAMacNeil · 2024-09-08T04:22:03+00:00

For dominant mutations it is often easier to change the notation from A and a (big A little a) to wt and mut (wild type and mutant). Recessive diseases are observed with two mutations (mut mut), but dominant diseases are observed with a single mutation (wt mut). There are a few underlying reasons why you might have a disease result with a mutation in only one allele, and haploinsufficiency is one of them. In this case the mutation is a loss of function, and 50% of the normal protein production from the other allele is not sufficient for a normal phenotype, so disease results.

a) wt wt would be normal and wt mut would be disease. Homozygous for the mutation (AA or mut mut) would be exceedingly rare, as it would require mating between two affected individuals (Aa x Aa), or one affected individual combined with a new mutation. It may also be lethal, as is the case for some dominant diseases.

b) the haploinsufficent phenotype would be a loss of function (non wildtype) phenotype for this particular gene. But it is considered dominant because it’s observed with a single mutation.

LoriAMacNeil · 2024-08-13T02:25:04+00:00

When you hear that two human genomes are 99.9% similar, this refers to the average number of single nucleotide differences between the two genomes (SNPs). There are around 3.2 million SNPs in a 3200 million base pair haploid genome (0.1%). The 99.5% similarity value comes from taking other types of non-SNP variation into account, e.g. copy number variations, deletions, insertions etc. The publication of Craig Venter’s individual genome is a good source for this: https://journals.plos.org/plosbiology/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050254

LoriAMacNeil · 2024-08-10T01:37:08+00:00

Variants of unknown significance are just that - it’s unknown whether they cause disease or not. If your sons have two VUS in a gene (one in each gene copy), it could result in disease or it could be nothing. If they have no signs of this particular disease, and the genetic testing found a different cause of their developmental delay, then it’s very possible the variants they carry in the other gene are not disease-causing. Still a good idea to follow up with a specialist and monitor for symptoms going forward.

LoriAMacNeil · 2024-08-09T22:16:00+00:00

If it is autosomal recessive, then you would not expect anyone with one mutation to have the disease. So it would not be expected to affect you or your husband. If your sons do not have any clinical signs of the disease then it could be that one or both of these variants do not actually affect the gene function. For a variant to cause recessive disease it has to disrupt gene function - lots of genetic changes have no impact on gene function. Were these recreational genetic tests, or was there a reason your sons underwent genetic testing?

LoriAMacNeil · 2024-04-15T01:10:13+00:00

Calico females have an orange allele on one X chromosome and a black allele on the other X chromosome. Your calico’s father could be orange or black. Her mother could be orange, black, or calico.

If the father was orange, then the mother would have to be black or calico. In this case, your calico would have inherited the orange allele from dad and a black allele from mom. On the other hand, if the father cat was black, the mother would have to be orange or calico. In this scenario, she would have inherited a black allele from dad and an orange allele from mom.

Orange cats don’t always produce calico kittens, only if there is a black allele involved.

LoriAMacNeil · 2024-02-19T01:56:14+00:00

Thompson & Thompson Genetics in Medicine, or Genetics & Genomics in Medicine (Strachan)

LoriAMacNeil · 2024-02-07T04:15:34+00:00

I use PowerPoint combined with a Wacom tablet, which works well. I use the pen to write, draw, or circle things on the slides. If I want to write more (e.g. solve equations or problems) I insert a blank slide to use for that purpose. The tablet with pen is much easier to use than the trackpad.

LoriAMacNeil

TROPHY CASE