zoology - Why do ants live so long?

There will always be a tradeoff in terms of resource allocation between reproduction and self maintenance. Since worker ants forego reproduction to perform other roles (gathering resources, caring for young etc.) within the colony, it makes sense that this would favour a longer lifespan. This idea works for most animals (i.e. higher reproduction = lower lifespan across species in general) and is well documented (Partridge et al. 1987, Gems & Riddle 1996 (PDF link), Westendorp & Kirkwood 1998 - to name a few). However the relationship is reversed in eusocial animals: the queens of ants, some bees and naked mole rats (which are all eusocial) tend to be longer lived than their sterile workers (Hartmann & Heinze 2003). Aging patterns within ants and other eusocial organisms are a very popular research topic at the moment, but the mechanisms causing differences between social castes are not fully understood.

Eusociality is strongly associated with increased lifespan, indeed many studies on the evolution of aging have focussed on eusocial animals which have appeared to overcome aging effects to an extent (Keller & Genoud, 1999, Buffenstein 2005). The naked mole rat is one of very few species of eusocial mammals and the relationship between its lifespan and body mass is very dissimilar to that of other rodents (ignore the bat points):

Image from Buffenstein & Pinto (2009).

If a queen has a longer reproductive lifespan then over the course of its life it will create a higher number of offspring. This will cause their increased longevity genes to be more prevalent in the gene pool over time - as long as they are able to reach the limit of their reproductive lifespan and are not killed by externalities (accident or attack) in the meantime. Therefore this trait (longer reproductive lifespan) will be selected for as long as the queen is protected.

Within eusocial colonies, there is often a protective environment (Buffenstein & Jarvis 2002): there is usually a physical structure (nest or burrow); symbiotic bacteria and/or fungi creating a more hygienic microflora; and queens are also protected by other castes. This gives queens a lower incidence of death due to accident or attack which (from the reasoning in the previous paragraph) supports the selection of a longer reproductive life. This is likely to lead to longer lived workers since they share the same genes.

However queens do tend to live much longer than their workers (O'Donnell & Jeanne 1995). This is probably due to their reproductive role. All the ants in the colony are investing in reproduction (whether by physically giving birth to young or by providing it with food and protection) therefore the normal relationship (reproduction and lifespan tradeoff) mentioned at the start is not relevant, but since the queen is the only individual reproducing, it will be the only one for whom lengthened lifespan is beneficial evolutionarily.

A mean lifespan of 20 years has been observed in Formica exsecta, and a maximum lifespan of 28.5 years observed in Lasius niger. Pogonomyrmex owyheei has an observed maximum of 30 years, and mean of 17 years. These (and many more) figures were obtained from a review by Keller (1998).

Other references on this subject include (Svensson & Sheldon 1998), (Keller & Genoud 1997) (PDF link), (Calabi & Porter 1989), and (Amdam & Omholt 2002).

References

• Amdam, G.V. & Omholt, S.W. (2002) The Regulatory Anatomy of Honeybee Lifespan. Journal of Theoretical Biology, 216, 209–228.




• Buffenstein, R. (2005) The naked mole-rat: a new long-living model for human aging research. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 60, 1369–1377.




• Buffenstein, R. & Jarvis, J.U.M. (2002) The Naked Mole Rat--A New Record for the Oldest Living Rodent. Sci. Aging Knowl. Environ., 2002, pe7.




• Buffenstein, R. & Pinto, M. (2009) Endocrine function in naturally long-living small mammals. Molecular and cellular endocrinology, 299, 101–111.




• Calabi, P. & Porter, S.D. (1989) Worker longevity in the fire ant Solenopsis invicta: Ergonomic considerations of correlations between temperature, size and metabolic rates. Journal of Insect Physiology, 35, 643–649.




• Hartmann, A. & Heinze, J. (2003) Lay eggs, live longer: division of labor and life span in a clonal ant species. Evolution, 57, 2424–2429.




• Keller, L. (1998) Queen lifespan and colony characteristics in ants and termites. Insectes Sociaux, 45, 235–246.




• Keller, L. & Genoud, M. (1997) Extraordinary lifespans in ants: a test of evolutionary theories of ageing. Nature, 389, 958–960.




• Keller, L. & Genoud, M. (1999) Evolutionary Theories of Aging. Gerontology, 45, 336–338.




• O’Donnell, S. & Jeanne, R.L. (1995) Implications of senescence patterns for the evolution of age polyethism in eusocial insects. Behavioral Ecology, 6, 269–273.




• Svensson, E. & Sheldon, B.C. (1998) The social context of life evolution history. Oikos, 83, 466–477.

genetics - Paralogous genes in genome-wide association studies?

Has anybody tested if paralogous genes are over-represented among the genes identified by genome-wide association studies (GWAS)?

For example, if a GWAS study finds 200 genes associated to the disease/trait, and a number X of those can be classified as belonging to Y different gene families, is there a test to see if X and Y are bigger than expected, given the total number of genes and gene paralogies in a genome? Here I am talking long established copies within a species, not CNVs in different individuals of the same species.

I am thinking there is an interesting question behind this: if a gene has duplicated during the evolution of a genome, and the different gene copies have taken specialized, yet related, roles, an unbiased analysis like GWAS should be able to find cases where different paralogous copies associate to different subdiseases/subtraits within the same global disease/trait.

pharmacology - How does Iota-Carrageenan achieve an antiviral effect?

Through two different pathways, one relying on a non-specific (innate) response, and another through a reactive oxygen species, the level of NF-kB^(**) is amplified, as such a response would have happened as a result of the presence of the virus anyway.

In thousands of experiments, carrageenans have been used to
induce inflammation, since inflammation is a predictable effect of
exposure to carrageenan in animal and cell-based models. For the
most part, these experiments were designed to test the effectiveness of anti-inflammatory agents or to study the mediators of inflammation

The innate immune pathway is mediated by toll-like
receptor (TLR)-4 and B-cell leukemia lymphoma (BCL)10, leading
to increased Interleukin (IL)-8 secretion by both canonical and noncanonical pathways of NF-kB activation. The ROS-mediated
pathway of inflammation does not involve TLR4-BCL10, but
requires Hsp27 and IkB-kinase (IKK)b, leading to increased phosphorylation of IkBa, and thereby enabling the nuclear translocation
of NF-kB.

From the intro to:

Yang B, Bhattacharyya S, Linhardt R, Tobacman J. (2012) Exposure to common food additive carrageenan leads to reduced sulfatase activity and increase in sulfated glycosaminoglycans in human epithelial cells. Biochemie, Mar 5,epub ahead of print, doi

(As an aside, the direct conclusions of this study are that these changes in GAGs may further influence transcription and play a role in determining cell fate, and perhaps may influence cell/cell interactions)

(**)NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls the transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens wiki

homework - Finding exons in DNA problem

After an RNA has been transcribed, in eukaryotes it is spliced before it leaves the nucleus. This means that parts of the RNA are removed (called introns) and the ends are capped. The parts left over in the mature mRNA after removing the introns are called exons.

The mRNA does not have to start with a start codon. There can be sequences before and after the bit which actually gets translated.

Yes, only one strand of DNA is transcribed into RNA. When you look at the mature mRNA below, read the first few bases and try to find their complements in the original DNA because this is where they were transcribed from. UCAUG is transcribed from the DNA AGTAC (with TCATG on the opposite side).

Now you look for the end of the mRNA. Bear in mind that all the A's are the poly-A tail which is added during splicing and determines how long the mRNA will persist in the cytoplasm. So you look for CUAGG in the original DNA, which must be transcribed from GATCC (with CTAGG on the opposite strand).

As you can see, that's exactly where the two red boxes start and end.

Now since the mRNA you see here is mature (indicated by the poly-A tail and the 5'-cap), that means introns have already been taken out. So any bases that you can see in the DNA between the start and end that we just found but not in the mRNA must have been an intron. Or the other way round: all the bases that are in the mRNA which you can also find in the DNA must be exons.

You will notice that exactly the bit that isn't in the red boxes doesn't appear in the mRNA anymore. Or: All of the mRNA is in the red boxes. The sequence is interrupted by a short bit which you can't find in the mRNA anymore - so this must be an intron.

What is the biology behind a skin "mole"?

A mole is simply a benign tumour, i.e. a proliferated cell growth that hasn’t become cancerous. So moles are not dead cells, they are very much alive. The colour is caused by a high concentration of the melanin, which is also responsible for normal darker skin.

Since moles are tumours, they can – but in most cases don’t – give rise to melanomas, malignant skin tumours, when they lose susceptibility to cell growth regulation and start invading surrounding tissue.

Scar tissue is entirely unrelated and due to regular regrowth of epithelial cells after injury forming a linear collagen structure (as opposed to the skin’s normal collagen structure, which resembles a “weaved“ structure).

human biology - Does the oxygen concentration equilibrate between red blood cells in the liver sinusoids?

The oxygen saturation (in lungs) and desaturation (in target organs) takes place via diffusion along the concentration gradient (i.e. partial pressure for gases). Therefore as long as RBCs from two different sources and having different partial pressure of oxygen mix up, the oxygen level starts to equilibrate between these cells.

But diffusion as a passive mechanism is not very fast and can take some time. So the only possibility for the second variant (there is a mixture of two types of RBCs) is if the mixture exists for very short time in liver sinusoids, so that the blood leaves them without really mixing completely up.

This is not true, at least in some animal models the blood within the liver seems to reach equilibrium very quickly and its resulting partial pressure can be influenced by adjusting the blood flow from different sources (using vasoactive substances injected directly, as in the referenced paper).

evolution - What do we know about the Last Universal Common Ancestor (LUCA)?

Carl Woese has much to say on this subject, including:

“The ancestor cannot have been a particular organism, a single
organismal lineage. It was communal, a loosely knit, diverse
conglomeration of primitive cells that evolved as a unit, and it
eventually developed to a stage where it broke into several distinct
communities, which in their turn become the three primary lines of
descent [bacteria, archaea and eukaryotes].”

There is a 2000 Scientific American article by W.F. Doolittle that discusses much of Woese's (and others') work understanding this question.

Also, see a couple of Woese articles here and here.

What specific membrane adaptations do cells have for saline-rich environs?

This 1969 Steensland paper seems to suggest that the membranes of halophiles are stabilized by sodium ions and they rapidly denature at lower-salt conditions (2.2 vs. 4.3 M). The protein composition of the membrane was generally acidic, stabilized by all the Na⁺.

As far as what the role of the halophile membrane is in sheltering the cell from the high ionic strength solution seems left unsaid.

immunology - Why do people dying of immune deficiency diseases appear sick?

Please forgive the obviously silly appearance of this question, and/or of the tenor which may come across as flippant or dismissive of real world suffering. My intention is none of the above.

As a layperson, I have always understood that the expression of our various colds/flus etc, while frequently mis-understood as being caused by the virus, are actually just manifestations of our own immunity fighting same. In other words, all the snot, and fever and inflammation are not caused *by the virus, they are a reaction *to the virus, as we fight it off.

My question then is why do people with AIDS (or similar immunity destroying affliction) appear sick? If they have weak or non-existent immune systems, following the above logic, would one expect to see them passing away while looking entirely healthy?