Findings

Leaf Fever
What are hotter: the needles of a black spruce in chilly Canada, or those of a Caribbean pine in sultry Puerto Rico?  For decades, plant biologists would have given the same answer as a sensible sixth-grader—“The ones in the tropics, dummy.”  Leaf temperature has long been thought to depend closely on that of the surrounding air.

But a recent finding by biology professor Brent Helliker, published in Nature, turns that conventional wisdom upside-down.  It turns out that black spruces and Caribbean pines have the same average leaf temperature—as do the 37 other tree species his team studied, ranging across 50 degrees of latitude.  They concluded that tree photosynthesis most likely occurs when leaf temperature is about 70 degrees Fahrenheit, and that different species have evolved strategies to maintain that temperature independent of ambient conditions.

“Our research suggests that they use a combination of purely physical phenomena—like the cooling from water evaporation or the warming caused by packing a lot of leaves together—to maintain what looks like leaf-temperature homeostatis,” Helliker says.

That sheds light on why certain trees grow in certain climates.  The finding also has repercussions for weather-prediction models, which rely on accurate measurements of surface water evaporation.  Additionally, it suggests that trees in northern latitudes may have it particularly rough in a warming world, as the mechanisms they’ve developed to warm their leaves potentially lead to overheating.

 

Salvation Through Mutation
They are few and far between, but people with a mutation in a gene called CCR5 are immune to HIV infection.  The protein normally synthesized by that gene serves as a kind of gate on the surface of T-cells, through which the virus enters in order to replicate itself.  When it’s absent, the HIV contagion stalls.

Writing in Nature Biotechnology in June, researchers from the School of Medicine reported the successful use of a strategy that aims to produce this useful mutation by artificial means.  Led by Elena Perez, an assistant professor of pediatrics, the team employed a “zinc finger” protein to deliver a DNA enzyme to CCR5 genes in healthy human T-cells.  The enzyme cut out a portion of the gene, giving rise to a mutation during the repair process that rendered the protein-synthesizing component nonfunctional. 

They then transferred the engineered cells to immune-deficient mice infected with HIV.  “We followed them over time and showed that those mice that received the zinc-finger-treated cells showed less viral load than controls, and improved CD4 [T-cell] counts,” says Perez, who is now planning a clinical trial in humans.

 

The Case for Naptime
Based on an experiment on mice, researchers at the School of Medicine suggested that inadequate sleep among elderly people may exacerbate cellular aging, potentially increasing their risk for diseases like Alzheimer’s and Parkinson’s.  The study focused on the unfolded protein response (UPR), an adaptive response to sleep deprivation which protects against the accumulation of misfolded proteins at the cellular level.  While UPR functioned adequately in the brain cells of young, sleep-deprived mice, it failed to do its job in old, sleep-deprived mice. 

The study, published in the June issue of the Journal of Neuroscience, indicated that sleep deprivation exacerbates other deleterious effects of aging in mice.  “We could speculate that sleep disturbance in older humans places an additional burden on an already-stressed protein-folding and degradation system,” says lead author Nirinjini Naidoo, an assistant professor in Penn’s division of sleep medicine.—T.P.