molecular biology - Why is propanoic acid often added to the diet of C. elegans?

Propanoic acid is toxic against many types of mold, fungi and bacteria (wiki), but same time has almost no effect to C. elegans ("fivefold less", reference). This is why propanoic acids and (more commmon) its salts are used as conservants for C.elegans cultures (as well as for other animals, like Drosophila).

botany - How can a monocot get so massive?

The vascular system is different in monocots and dicots. In dicots the vascular tissues are arranged in concentric circles; one of these rings is meristematic cells (undifferentiated cells that can differentiate into any cell type). This ring of meristem tissue is called the vascular cambium and is where secondary growth occurs - xylem grows inwards and phloem grows outwards.

Whereas:

Monocots have a distinctive arrangement of vascular tissue known as an
atactostele in which the vascular tissue is scattered rather than
arranged in concentric rings. Many monocots are herbaceous and do not
have the ability to increase the width of a stem (secondary growth)
via the same kind of vascular cambium found in non-monocot woody
plants. However, some monocots do have secondary growth, and because
it does not arise from a single vascular cambium producing xylem
inwards and phloem outwards, it is termed "anomalous secondary
growth". (Wikipedia)

For palms specifically:

Palm trees increase their trunk diameter due to division and
enlargement of parenchyma cells, which is termed diffuse secondary
growth. (Wikipedia)

Parenchyma cells are type of cells found in plant ground tissue, which makes up the bulk of plant mass.

genetics - Are there any DNA base sequences that are fully conserved between the genomes of all humans?

In 2004 Bejerano et al. identified "481 segments longer than 200 base pairs (bp) that are absolutely conserved (100% identity with no insertions or deletions) between orthologous regions of the human, rat, and mouse genomes". These were found to be mostly in/around genes related to RNA processing, which is perhaps unsurprising given that it is such a primitive/inherent biological process.

Bejerano's paper has been cited over 500 times on Scopus, with numerous papers reporting variants in such regions that cause diseases such as colorectal adenocarcinomas.

---

So few conserved regions exist because there is plenty of redundancy in the genome; many genes functionally overlap with others, and many genetic variants are 'silent' - they have no effect on the phenotype. Having this variability is advantageous in Darwinian terms because this increases the evolvability of the species.

There are many regions of very high homology between individuals (protein-coding regions are highly conserved even between species), but there will still be natural variation; each mutations effect will be dependent on the rest of the genome. Genes work together to produce a working organism - they do not each code for a little 'bit', and therefore a change in one portion of the DNA may be 'balanced' by a change elsewhere.

It is only in 'ultra-conserved' sequences that mutations are presumably incompatible with life because the process is so finely-tuned and indispensable.

evolution - Can species back-evolve?

Just to clarify, as one might read your question as if humans had evolved from dogs - humans and dogs have a common ancestor, one is not a direct descendant of the other.

In terms of evolution running backwards, it has actually been experimentally tested in microorganisms, where you can check the phenotype (characteristics) of an organism over hundreds and thousands of generations. One example that comes to mind is Joe Thornton's research where he reconstructed a gene for an ancient protein and compared it to the more modern versions. They found out that the key mutations that modified the protein sequence could not be simply changed back to obtain the more ancient form, because in the meantime many neutral mutations had accumulated in that protein and while they did not change the protein sequence, they interacted with the protein-changing mutations and prevented the de-evolution of the protein.

The paper I have in mind (there are many more on this) is: Bridgham, Jamie T, Eric A Ortlund, and Joseph W Thornton. 2009. “An Epistatic Ratchet Constrains the Direction of Glucocorticoid Receptor Evolution.” Nature 461 (7263) (September 24): 515–519. doi:10.1038/nature08249.

On the other hand, in a sort of more esoteric example (as it is not directly de-evolution), blind cavefish have multiple mutations (and sometimes in multiple genes) that cumulatively result in loss of vision. Let's then say you have population of the fish that have sight-losing mutations in gene A and another population with mutations in gene B. Both populations are blind, but if you could cross the fish from the two populations, the eye-loss mutations in genes A and B would be substituted by 'correct' versions from the other population and thus both fish would be able to see again. While not de-evolution in itself, it shows that for relatively simple changes that were not influenced by other changes in the genome, you can rewind the clock and get the long-lost phenotypes, even like the sight.

See here: Borowsky, Richard. 2008. “Restoring Sight in Blind Cavefish.” Current Biology : CB 18 (1) (January 8): R23–4. doi:10.1016/j.cub.2007.11.023. (this is a description of the research, not the actual paper; but it links to it).

Both these examples are super-cool (IMHO), and in my collection of all-time favorite evolutionary stories. But practically speaking, what you're asking for (from humans and dogs to their most common ancestor) is not possible. Too many variables (both genetic and environmental and stochastic) to control. The papers are behind the paywall, but if you want them, send me an email.

How high is the energy yield of photovoltaics compared to photosynthesis?

According to wikipedia, plants typically convert around 5% of the energy of the sunlight that hit the leaves into energy usable by the plant. Sugarcane seems to be the best, it converts up to 8% of the energy into actual biomass.

The best solar panels on the market, according to the Independent, convert 21% of energy from sunlight into usable electricity. Experimental prototypes do much better, and there are some that get over 40%. Wikipedia has a nice graph of the most efficient solar cell prototypes.

senescence - How does the NAD+/NADH ratio affect lifespan in vertebrates?

Here's the proximate physical implication of the ratio (from the Wikipedia article on NADH).

The balance between the oxidized and reduced forms of nicotinamide
adenine dinucleotide is called the NAD+/NADH ratio. This ratio is an
important component of what is called the redox state of a cell, a
measurement that reflects both the metabolic activities and the health
of cells. The effects of the NAD+/NADH ratio are complex,
controlling the activity of several key enzymes, including
glyceraldehyde 3-phosphate dehydrogenase and pyruvate dehydrogenase.
In healthy mammalian tissues, estimates of the ratio between free NAD+
and NADH in the cytoplasm typically lie around 700; the ratio is thus
favourable for oxidative reactions. The ratio of total
NAD+/NADH is much lower, with estimates ranging from 0.05 to 4. In
contrast, the NADP+/NADPH ratio is normally about 0.005, so NADPH is
the dominant form of this coenzyme. These different ratios are key
to the different metabolic roles of NADH and NADPH.

So here's my question: how does this manifest in vertebrate aging? Is it something that's simply the resultant of other aging processes, or can the ratio also contribute to aging in a certain way?

human biology - In which order did the cells of the immune system evolve?

As I'm lucky enough to have access to that article, I'm going to extract whatever I can find to answer your question.

To begin with, innate immunity must have evolved first - we can see it at almost all stages of evolution. According to Cooper & Herrin, ever since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms.

They state that around 500 million years ago, the first adaptive immune systems evolved in vertebrates, but do not explain how although they attempt to. Instead, they explain why we are not able to discern at the moment how this evolution came about. The main reason given is that it is unknown when some key cells evolved (namely natural killer cells and dendritic cells) Additionally, mice and humans evolved two different kinds of natural killer cell receptors relatively recently while sharing a common ancestor only quite a long time ago.

Apparently jawed and jawless vertebrates have also evolved two different kinds of adaptive immune systems. They both seem to rely on the same mechanisms but on a different molecular and genetic basis. Cooper & Herrin conclude that at the current level of research, we are not able to determine the evolution of our immune system.

Source: How did our complex immune system evolve?

Personally, if I'm allowed to give in to the temptation of speculation a bit, I would go by a similar strategy as the evolution of Krebs cycle - look which bits make sense even without the rest. There is of course the major obstacle that the cells of the immune system require an entirely new branch in haemopoiesis: all innate immune cells (aside from natural killer, NK cells) derive from the common myeloid progenitor, whereas all adaptive immune cells (and NK cells) derive from the common lymphoid progenitor.

I think this may even be a first hint: NK cells are innate immune cells but they derive from a different lineage at the highest level - they may have evolved as the first lymphoid cells after the myeloid innate immune cells. The next closest related cell is the cytotoxic T cell (CD8+, aka Tc), which utilises the exact same killing mechanisms (perforin+granzymes and Fas ligand) and attaches to other cells in almost the same way as the NK cell (immune synapse). It is also independent and can kill on its own, as long as it recognises its specific antigen. This is the main difference and also a very large step - the generation of the specific T cell receptor. Once the specific T cells receptor is developed, the step to helper T cells (CD4+, Th) is not far, although these perform a relatively bystander-like role in the immune response, steering the other immune cells from behind the scenes and not directly effecting any killing of the pathogen. Therefore I would guess that before helper T cells, B cells evolved, which are capable of producing antibodies. Antibodies themselves are very similar to the T cell receptor (not in gross structure but in the underlying genetic domains and their processing), so a 'detachable' antigen-specific T cell receptor may have evolved and ultimately caused the development of a new cell type. Once all these components are present, it is necessary (or beneficial) to control which cell types are the most active and in which way they act at the site of infection. This is exactly what helper T cells do, by steering the local immune response either into a Th1 (cytotoxic) or a Th2 ('humoral', anti-parasitic) response direction.

botany - What's a good reference for choosing histological staining chemicals?

It's often difficult to find the appropriate or best stain to use when I want to examine a new type of tissue. I think that's partly because many histological techniques were developed a long time ago, so the papers don't turn up in Google Scholar. Is there a standard reference which links tissues, cell types or states and their corresponding best stain?

I'm mostly interested in a reference text or website covering plant histology, but general references are welcome too.

evolution - Why do pandas have a high probability of giving birth to twins?

Charnov and Ernest (2006) present data on offspring number per year and neonatal mass for 532 species of mammals. The two are related by the linear regression equation:

ln(offspring/year) = 2.4 - ( 0.3 * ln(neonate mass) )

Giant panda neonates weigh 100-200 g and are weaned at 46 weeks.

So, according to the regression, pandas should have, on average, 2.8 to 2.2 offspring per year (for 100 and 200 g respectively). With a weaning time of 46 weeks, they could have 1.13 (52/46) litters per year. If every litter were exactly twins, that would be 1.13 * 2 = 2.26 offspring per year, which is within the predicted range.

Humans (neonatal mass of 3400 g) are predicted to have 0.96 offspring/year.

Charnov EL and SKM Ernest. 2006. The Offspring‐Size/Clutch‐Size Trade‐Off in Mammals. American Naturalist 167:578-582.