Each of our cells has the same gene sequences

[glipsnort (Steve Schaffner)]

@Tomi_Aalto

Bacteria have a sense smell and quorum sensing.

True but irrelevant to genetic mutations that cause antibiotic resistance in bacteria.[quote=“Tomi_Aalto, post:36, topic:35836”]
They are able to rapidly adapt to changing environment due to epigenetic mechanisms (adenine methylation), alternate reading frame and by shuffling with genetic information inside the population.
[/quote]
All true, and all irrelevant to genetic mutations that cause antibiotic resistance in bacteria.[quote=“Tomi_Aalto, post:36, topic:35836”]
There are no beneficial random genetic errors within humans.
[/quote]
False.

[Tomi_Aalto]

@glipsnort

False.

Then why don’t you address me one?

[glipsnort (Steve Schaffner)]

@Tomi_Aalto

Then why don’t you address me one?

The A111T mutation in SLC24A5, which confers light pigmentation on Europeans. The V370A mutation in EDAR, which increases the number of eccrine sweat glands and hair thickness. Six different mutations in LCT that confer lactase persistence.

[cwhenderson (Curtis Henderson)]

I have nowhere near the detailed scientific knowledge @glipsnort possesses, but I know there are several mutations that provide malaria resistance to some extent.

[Argon]

Also CCR5Δ32, which confers resistance to HIV infection.

‘Beneficial’ and ‘deleterious’ are deeper terms with regard to mutations than most people think. The effects of variation are all context specific. It may be helpful to instead think of mutations that are subject to positive selection within a particular situation. The examples Steve Schaffner cites are variations that appear to have increased in certain populations because of positive selection for the alleles.

[jpm (Phil McCurdy)]

and I just saw this (speaking of questionable sources, but oh well):

Rare Gene Mutations Inspire New Heart Drugs (Published 2017)

[T_aquaticus]

@Tomi_Aalto

Then why don’t you address me one?

Take your pick from the 40 million mutations that separate humans and chimps.

[T_aquaticus]

@Tomi_Aalto

Bacterial genetic changes are not random occurrences. Bacteria have a sense smell and quorum sensing. They are able to rapidly adapt to changing environment due to epigenetic mechanisms (adenine methylation), alternate reading frame and by shuffling with genetic information inside the population.

The Lederberg’s were able to demonstrate that bacteria produced mutations conferring antibiotic resistance even when the bacteria had never been exposed to antibiotics. They started their experiment with a single bacterium, and then created their starter population from that single individual bacterium. They spread the starter population on an agar plate that did not contain antibiotics and let it grow into a thick lawn of bacteria. Using a Velcro stamp. they transferred bacteria from the antibiotic free plate to fresh antibiotic plates. A day later they say colonies of resistant bacteria on the antibiotic plates, but here is the interesting thing. The colonies on the antibiotic plates were at the same position on each plate. This means that the antibiotic resistant bacteria came from the same spot on the master plate that did not contain antibiotics. The mutation occurred on the master plate without antibiotics, and it was passed down clonally in the complete absence of antibiotics.

That is random mutagenesis. The mutations that produced antibiotic resistance occurred in the absence of antibiotics, contrary to the story you are trying to tell.

[T_aquaticus]

@Tomi_Aalto

Most genetic alterations are caused by disrupted methylation patterns. The most common type of substitution is 5mC>T, because glycosylase doesn’t repair that modification. For base pair pairing to be correct, it also leads to G>A substitution in the next replication procedure. But there are several other genetic mutations that are mostly caused by epigenetic reasons.

That doesn’t change the fact that mutations are observed to be random with respect to fitness.