genetics - Do trees age on a microscopic level?

I've been doing some reading, and have come up with the following interesting information.

Telomeres

During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess nucleotides – at the ends called telomeres (Silvestre, 2012).

Mammalian cells do not replenish their telomeres after cell division, giving them a replicative lifespan; a maximum number of cell divisions before the telomeres run out. The cells then either enter a state of senescence and no longer divide, or initiate programmed cell death. However each cell has the genetic information for telomerase – the enzyme that can replenish the telomeres – but cannot use it. Only embryos and stem cells are able to express telomerase in mammalian cells - this protects against the build up of damage to DNA causing uncontrolled cell cycle progression. Activated telomerase is a core feature of many cancers (Campbell, 2012).

Plant Telomeres

You mention telomeres in your question, and it is an interesting question I had never considered. Plants have no germline preserved, so their progeny must bear all the defects of their particular parent cell, and that plant cells must therefore all have the capacity to regenerate their telomeres. I found a paper by Fajkus and colleagues that finds telomerase activity in plant cuttings grown in culture (Fajkus, 1998). Their hypothetical Plant Telomere-Length Regulating (PTLR) protein must arise in the early stages of the culture and last only a few cycles. Interestingly it seems that the efficiency of this process varies between different plant species. The authors note that their plant of choice – tobacco – is particularly proliferative and that other plants such as barley were harder to grow from cuttings, which may be down to a different way of regulating the telomerase (for instance it could only be activated occasionally at low amounts).

Do Plants Get Cancer?

It seems to me the next obvious question. One of the first papers I came across (published in 1916 by the Journal of Cancer Research!) talks of Crown Gall in plants and its relation to human cancer (Smith, 1916). Many websites cite galls as being the equivalent to cancer in plants, but it appears that the outgrowths (galls) that appear very tumour-like are in fact caused by bacteria encouraging their surrounding cells to proliferate. (See this question for more detail on galls).

I later found an abstract (I cannot access the full paper) from a paper published in Nature in 2010 called “Walls around tumours — why plants do not develop cancer” (Doonan, 2010). It appears that Plants can and do develop tumours, but they are less frequent and less lethal due to fundamental differences in development between plant and animal cells. Singh and colleagues found that in 2 plant species (Arabidopsis and rice) there were DNA damage repair pathways well conserved but with variation; there were several gene duplications in different DNA repair pathways (Singh, 2010).

Plants Do Not “Age” As We Do

Although I could find no conclusive evidence, it seems to me likely that plants may also have enhanced maintenance against other cellular stresses than DNA damage, such as build-ups of aberrant proteins. It therefore appears that in a protected environment some plants could live indefinitely. I say some, because others deliberately end their lives after reproduction. Traits such as longevity are inherently hard to be selected for, as the advantages come long after reproductive maturity and are therefore under much less selective pressure.

We see plants wither and die, but this is because they are constantly subject to environmental insult. Animals and insects may eat them, there may not be enough food or water, or sunlight, or the plant may become infected. All of which are at the macroscopic level. Due to completely different evolutionary constraints and pressures plants are highly resilient to cellar stresses, possibly due to differences in metabolic rate, and apparently have indefinite replicative potential.

Edit:
Although the more I think about it, the more it seems that most plant must have an ultimate lifespan, in that as they forever grow and expand their tissues would gradually harden and become less functional (I am mostly imagining bark plants here). Although as the layers of bark are pushed out the layers below take the place. In this way a tree could possibly live indefinitely by continuously remodelling it's layers.

molecular biology - Why are restriction enzymes not frozen?

It's just so much more convenient to have the enzymes ready without having to thaw them. The main reason you freeze enzymes is to keep them active, if you figure out a buffer that keeps them unfrozen without compromising activity, that is a huge increase in convenience.

Not having to thaw the enzymes before use saves a lot of time, if you can manage to keep the enzymes active in those non-freezing conditions that is a clear advantage.

Glycerol also stabilizes proteins in solution, and multiple freeze and thaw cycles can negatively affect enzyme activity for some enzymes.

human biology - What causes the development of antibiotic-resistant strains of bacteria?

The lead question you have answered yourself: bacteria become resistant because of the selection pressure caused by the antibiotic's effective suppression of the original non-resistant bacteria. Those variants which resist the suppression are selected for as a natural consequence.

How do resistant bacteria process antibiotics? It depends on the details of the particular antibiotic, and perhaps the kind of resistance.

Take the case of penicillin and related antibiotics, like amoxicillin. These antibiotics act by inhibiting the formation of a layer of the cell wall which is essential for many kinds of bacteria. This prevents multiplication of the bacteria and contributes to their distruction. Wikipedia gives some details on the action of these β-lactam antibiotics.

Bacterial resistance to drugs like penicillin usually takes the form of the bacteria producing an enzyme (called β-lactamase) which breaks apart a ring in the drug molecule, disabling it and thus removing its effect on cell wall synthesis.

This resistance has become common because of the widespread use of penicillin-like drugs and because of transfer of the gene for it between bacteria species as by plasmids.

Researchers managed in the 70s to discover and develop an auxilliary weapon in this war. This was clavulanic acid, which has a structure partly similar to the penicillins and like them is attacked by the bacterial β-lactamase enzyme. Unlike the penicilins though, it forms a permanent bond with the enzyme molecule, disabling its activity. This has led to currently effective drugs like Augmentin which include in the same pill both amoxicillin and its protector, clavulanic acid.

human biology - Death because of distilled water consumption

In general, if you want to know "exactly how much of X on an average is needed to be consumed to cause death", then the magic search term for Google is "LD50", that is the dose that kills 50% of victims.

I've seen the LD50 for distilled water quoted as 90ml/kg for rats (that is, 90 ml per kg of body mass). I presume that figure comes not from theorising about salt intake, but from giving measured quantities of distilled water to rats and counting how many die.

It's likely of the same order of magnitude for humans. Unlike many "poisons" it's not about subtleties of liver chemistry that will vary by species. What killed the rats was the swelling by osmosis of cells and tissues that they didn't want swelled.

For a largeish human that dose is 7 litres, approx 14 pints, drunk at a sitting. Which is fairly unlikely in a school chemistry lesson. Besides, with effort you could drown in less than that!

The distilled water in your chemistry lab has a relatively much larger chance of killing you for some reason other than its inherent toxicity (although it's still fairly unlikely in absolute terms). For example if it's stored for a while there could be legionella in the tanks. Probably best not to drink it, just as it's best not to drink any water that may have been sitting around for weeks in an unsealed container.

Definitely don't drink other stuff from the labs that your friend tells you is poisonous, because some of it really is. In particular the one everybody thinks of (because, like the water, it's similar to something they know about): lab ethanol can have methanol as an impurity, and may well have had benzene intentionally added because that's an easy way to get the last 4.5% water out that otherwise cannot be removed by distillation. A mouthful of ethanol isn't normally lethal (although it might be illegal), whereas methanol and benzene are both "properly" toxic in the sense that a few grams will kill you.

By the way, I can confirm that in my school days I obtained the same experimental result you did.

human biology - Is there any advantage to one blood type over another?

I've been doing a little more digging myself and have found a couple of other advantages:

Risk of Venous-thromboembolism (deep vein thrombosis/pulmonary embolism ⁽¹⁾). Blood group O individuals are at lower risk of the above conditions due to reduced levels of von Willebrand factor⁽²⁾ and factor VIII clotting factors.

Cholera Infection Susceptibility & Severity. Individuals with blood group O are less susceptible to some strains of cholera (O1) but are more likely to suffer severe effects from the disease if infected ⁽³⁾.

E. coli Infection Susceptibility & Severity. A study in Scotland indicated that those with the O blood group showed higher than expected infection rates with E. coli O157 and significantly higher fatality rates (78.5% of fatalities had blood group O).⁽⁴⁾

Peptic Ulcers caused by Heliobacter pylori which can also lead to gastric cancer. Group O are again more susceptible to strains of H. pylori ⁽⁵⁾.

Whether blood group antigens are displayed on other body cells or not has been linked to increased or decreased susceptibility to many diseases, notably norrovirus and HIV. This is fully explained in the article that I was above summarising - "The relationship between blood group and disease" in addition to extended descriptions of the other two answers.

evolution - Why does the butterfly have a cocoon stage in its life cycle?

Holometaboly is believed to have evolved only once (Labandeira, 2011), but is arguably the most successful mode of development we know of in terms of species richness (Kristensen, 1999 - PDF link). Insects which have adopted this method are far more diverse than their hemimetabolous counterparts. A conservative estimate by Hammond (1992) is that holometabolous insects comprise more than 60% of all living organisms.

The subclass Pterygota (winged insects) is divided into (super orders) endopterygota (wings develop interiorly) which are holometabolous, and the exopterygota (external wing development) which are hemimetabolous.

Hemimetabolous insects (usually) develop from an egg to an adult through a series of immature forms (known as nymphs or instars) which are slightly modified (and usually slightly larger) forms of the preceding form. There are exceptions to this mode within the exopterygota including asexual parthenogenesis which is common in aphids. The general life cycle is well illustrated in the Dermaptera (earwigs). All stages inhabit the same ecological niche and so maintain the same general body plan.

Image file from Wikimedia Commons here

Although hemimetaboly is a more gradual process than holometaboly, it happens in a small number (often four or five nymphal instars) of discrete steps rather than the more continuous development of other animals such as mammals. Although all insects fall into either the exopterygote or endopterygote categories (i.e. wings either develop externally or internally), there are examples of intermediate processes which lie somewhere between hemi- and holometaboly. A notable example are the Cicadas. Cicadas are Hemiperans (true bugs) which lie in the exopterygota and so are, by default hemimetabolous. However there is a considerable difference between their immature and mature stages:

Illustration by Debbie Hadley, using drawings from Insects - Their Ways and Means of Living by Robert Evans Snodgrass, U.S. Bureau of Entomology. These drawings are in the public domain. From here.

During the immature stages, the larva (or nymph) will burrow underground, sometimes for many years. This requires strong front appendages, which they also use when they surface to grip onto a surface whilst they shed their final skin to become an adult. This differential niche exploitation is likely to have given rise to the morphological differences between immature and mature life stages.

Exploiting different niches during different developmental stages not only reduces intra-specific competition between young and adult, it also enables the insect to be more specialised to fulfill their specific role, which changes as they develop. The role of the immature is to grow, they do not yet need to be able to reproduce or disperse; whereas the role of the adult is to find a mate and reproduce. Young often develop below ground where there are fewer predators, adults often fly to enhance dispersal (further reducing competition and also decreasing inbreeding). These two activities call for vastly different body designs.

Some other common holometabolous insect orders are Coleoptera (beetles), Hymenoptera (bees, wasps, and ants), and Diptera (true flies), whereas hemimetabolous groups include Orthoptera (grasshoppers, crickets etc.), Mantodea (praying mantids), and Blattaria (cockroaches).

As for the chrysalis which Lepidoptera (butterflies and moths) have evolved to surround their pupal stage, the main role is likely to be protection. Larvae (caterpillars) are a highly nutritious and energetic food source and thus have adapted defensive mechanisms such as mimicry, warning colours, and dropping to the ground when disturbed. This drop would damage the metamorphosing pupa (the most vulnerable stage as it is usually relatively immobile), as the cuticle softens to allow for cell-rearrangement.

The process of insect development is regulated by juvenile hormone (JH), see Konopova et al, (2011) for more on this.

References

• Hammond, P. (1992) Species Inventory. Global Biodiversity (ed B. Groombridge), pp. 17–39. Chapman and Hall, London.




• Konopova, B., Smykal, V. & Jindra, M. (2011) Common and Distinct Roles of Juvenile Hormone Signaling Genes in Metamorphosis of Holometabolous and Hemimetabolous Insects. PLoS ONE, 6, e28728.




• Kristensen, N.P. (1999) Phylogeny of endopterygote insects, the most successful lineage of living organisms. European Journal of Entomology, 96, 237–253.




• Labandeira, C.C. (2011) Evidence for an Earliest Late Carboniferous Divergence Time and the Early Larval Ecology and Diversification of Major Holometabola Lineages. Entomologica Americana, 117, 9–21.