confessions of a biology nerd

Time is really the fourth dimension of living organisms. It enters as a part into the constitution of a tissue. Cell colonies, or organs, are events which progressively unfold themselves. They must be studied like history.
—  Alexis Carrel, from the epigraph to Culturing Life by Hannah Landecker

Images from the cover of the October 2011 issue of Nature Immunology.

DDX41, a member of the DExD/H-box helicase family, senses viral DNA and triggers type 1 interferon responses in a manner dependent on the adaptor STING, as reported by Liu and colleagues (p 959News and Views by Barber, p 929). DDX41 mutants that lack the STING-binding DEADc domain (green dots) fail to associate with cytoplasmic STING (red); DAPI stains the nucleus (blue). Original image by Musheng Bao (bottom). Artwork by Lewis Long (top). (source)

“Bacterial colonies learn. The response of the P. vortex bacteria to non-lethal levels of the antibiotic Septrin. The normal growth pattern in the absence of the antibiotic is shown in panel A. The effect of the first exposure is shown in panel B. The response in a second encounter is shown in panel C. The antibiotic stress induces the bacteria to intensify chemotactic attraction and form larger vortices. This clever strategy protects the bacteria since, as in larger vortices, the antibiotic is diluted by lubricating fluid they excrete. The bacteria enhance their repellent chemotactic signaling to push the vortices away from the antibiotic more rapidly. The ‘higher complexity for greater adaptability’ behavior is manifested in the fact that the growth pattern in panel B is less complex than that in panel A. Learning from experience is exemplified in panel C. Upon second encounter with the antibiotic the colony expands faster and the pattern is more complex.”

– Eschel Ben-Jacob, Yoash Shapira, and Alfred I. Tauber, “Smart Bacteria,” from Chimeras and Consciousness

“Laser confocal micrographs of stained chromatin showing superficial cleavage in a Drosophila embryo. The early nuclear divisions occur centrally. Numbers refer to the cell division cycle. At division cycle 10 (2 hours after fertilization), the pole cells form in the posterior, and the nuclei and their cytoplasmic islands (energids) migrate to the periphery of the cell. This creates the syncytial blastoderm. After cycle 13, the oocyte membranes ingress between the nuclei to form the cellular blastoderm.”

From Developmental Biology by Scott F. Gilbert; images courtesy of D. Daily and W. Sullivan.

“After the genome (epigenetics) : microarray analysis of patterns of gene switching. In this case, each spot corresponds to one of 6,000 different genes in Plasmodium falciparum, the cause of the severest form of malaria. In our search for a vaccine or cure, we need to know what genes are active in different phases of the life cycle. Here a red spot indicates a gene active in one phase but not another, and a green spot the opposite. Genes that are active in both phases tend to show up yellow.”

– James D. Watson, from DNA: The Secret of Life

Original antigenic sin, also known as the Hoskins effect, refers to the propensity of the body's immune system to preferentially utilize immunological memory based on a previous infection when a second slightly different version, of that foreign entity (e.g. a virus or bacterium) is encountered. This leaves the immune system “trapped” by the first response it has made to each antigen, and unable to mount potentially more effective responses during subsequent infections. The phenomenon of original antigenic sin has been described in relation to influenza virusdengue feverhuman immunodeficiency virus (HIV), and to several other viruses.

This phenomenon was first described in 1960 by Thomas Francis, Jr. in the article “On the Doctrine of Original Antigenic Sin”. It is named by analogy to the theological concept of original sin. According to Thomas Francis who originally described the idea and cited by Richard Krause:

“The antibody of childhood is largely a response to dominant antigen of the virus causing the first type A influenza infection of the lifetime. […] The imprint established by the original virus infection governs the antibody response thereafter. This we have called the Doctrine of the Original Antigenic Sin.”



Transmission electron micrograph of the magnetotactic bacterium  Aquaspirillum magnetotacticum [also classified as Magnetospirillum magnetotacticum strain MS-1] (first image, x123,000 magnification, with magnetic particles designated as ‘MP’), isolated magnetosomes (second image, x140,000 magnification), and bacteria migrating in waves when exposed to a magnetic field (third image), from Prescott, Harley, and Klein’s Microbiology, 4th edition. 

On magnetotactic bacteria, the authors of Microbiology note that “most of these bacteria have intracellular chains of magnetite (Fe3O4) particles that are called magnetosomes. Magnetosomes are around 35 to 125 nm in diameter and are bounded by a lipid bilayer […] Since each iron particle is a tiny magnet, the Northern Hemisphere bacteria use their magnetosome chain to determine northward and downward directions, and swim down to nutrient-rich sediments or locate the optimum depth in freshwater and marine habitats. Magnetotactic bacteria in the Southern Hemisphere generally orient southward and downward, with the same result. Magnetosomes are also present in the heads of birds, tuna, dolphins, green turtles, and other animals, presumably to aid navigation.”

For a long time, it was thought that the CCR5-delta32 mutation, which confers resistance to pathogens that infect macrophages (CCR5 is a chemokine receptor), like HIV, increased in frequency in European populations after the Black Death of the mid-14th century, because only individuals with at least one mutant allele had a chance of surviving the Yersinia pestis epidemic (Y. pestis infects macrophages).

Studies on ancient DNA suggest that the mutation may actually stem back to the Bronze Age, and perhaps even back to the age of Vikings. It turns out that members of the poxvirus family, like smallpox, exploit chemokine receptors on cell surfaces for purposes of viral attachment and entry, and smallpox has been a human problem for thousands of years, unlike HIV, which only emerged within the past century.

The mutation can confer “resistance” to HIV because while the virus can bind to its receptor (CD4) on macrophages, it cannot bind its coreceptor (CCR5) and thus cannot enter the cell to begin its replication cycle. Macrophage-tropic HIV is associated with increased virulence and disease progression because of the nature of the macrophage – as a phagocytic cell of the innate immune system, its role is to pass through the circulation (in its undifferentiated monocytic form) and tissue (as a differentiated macrophage) and engulf and digest things like pathogens and dead cells. 

For more, see Galvani and Novembre, The evolutionary history of the CCR5-delta32 HIV-resistance mutation (2005).

The C1 complex*, consisting of six C1q subunits, two C1r subunits, and two C1s subunits, is involved in the classical pathway of the complement system, a component of innate immunity that functions to recognize and target pathogens for destruction. C1q is capable of binding pathogens directly via molecular patterns on their surfaces or indirectly by binding the constant regions of antibodies bound to pathogens. C1r and C1s are proteases that, when activated, cleave the complement proteins C2 and C4 to generate the classical C3 convertase. This action ultimately leads to the deposition of opsonins, proteins that facilitate phagocytosis and degradation of the pathogen, on pathogen surfaces. 

Image via Janeway’s Immunobiology by Kenneth Murphy. The micrograph (magnification 500,000x) is courtesy of K.B.M. Reid. 

* See also: elegant flowerlike protein complexes


“The first description of the hippocampus was written by Arantius in 1587, who compared the protrusion on the floor of the temporal horn to a hippocampus, or seahorse (from Latin hippocampus, from the Greek hippokampos, in turn from  ἵππος, "horse” and κάμπος, “sea monster”). It should be noted, however, that he hesitated between the words ‘seahorse’ and 'silkworm’.“ 

From Henri M. Duvernoy's The Human Hippocampus, with slight modifications. See also: Hippocampus