Modeling the effects of proton irradiation [on] CIGS solar cells

The space environment is very harsh on photovoltaic devices. Solar protons (hydrogen ions) cause large numbers of vacancies, which act as recombination centers at deep levels and can create compensating defects that reduce the acceptor concentration at shallow levels in semiconductors. This in turn, can reduce the output power generated by photovoltaic devices. Damage can also occur from atomic oxygen, plasma discharges and electron irradiation. Solar arrays have to be manufactured to produce more power than necessary so that the solar array will still produce the needed amount of power after degradation occurring from charged particle irradiation. A major challenge is to be able to model these devices so that the effects of charged particle irradiation can be taken into account in calculations for the End of Life (EOL) open-circuit voltage, short-circuit-current, fillfactor,and efficiency. Models presently being used do not provide distinct values without more calculations. Also, models presently being used tend to have proton irradiation incident normal to the surface, which does not reflect actual conditions, and require a significant amount of input data. In an effort to correct these problems, a new model was created that finds the remaining factor of the normalized basic cell parameters for CuInGaSe2 (CIGS) solar cells. This model uses significantly fewer inputs than other computer models, provides a more realistic model with respect to entry angles of incident protons, and provides actual and normalized values without extra calculations

The intrinsic chaperone network of Arabidopsis stem cells confers protection against proteotoxic stress

The biological purpose of plant stem cells is to maintain themselves while providing new pools of differentiated cells that form organs and rejuvenate or replace damaged tissues. Protein homeostasis or proteostasis is required for cell function and viability. However, the link between proteostasis and plant stem cell identity remains unknown. In contrast to their differentiated counterparts, we find that root stem cells can prevent the accumulation of aggregated proteins even under proteotoxic stress conditions such as heat stress or proteasome inhibition. Notably, root stem cells exhibit enhanced expression of distinct chaperones that maintain proteome integrity. Particularly, intrinsic high levels of the T-complex protein-1 ring complex/chaperonin containing TCP1 (TRiC/CCT) complex determine stem cell maintenance and their remarkable ability to suppress protein aggregation. Overexpression of CCT8, a key activator of TRiC/CCT assembly, is sufficient to ameliorate protein aggregation in differentiated cells and confer resistance to proteotoxic stress in plants. Taken together, our results indicate that enhanced proteostasis mechanisms in stem cells could be an important requirement for plants to persist under extreme environmental conditions and reach extreme long ages. Thus, proteostasis of stem cells can provide insights to design and breed plants tolerant to environmental challenges caused by the climate change

In planta expression of human polyQ-expanded huntingtin fragment reveals mechanisms to prevent disease-related protein aggregation

In humans, aggregation of polyglutamine repeat (polyQ) proteins causes disorders such as Huntington’s disease. Although plants express hundreds of polyQ-containing proteins, no pathologies arising from polyQ aggregation have been reported. To investigate this phenomenon, we expressed an aggregation-prone fragment of human huntingtin (HTT) with an expanded polyQ stretch (Q69) in Arabidopsis thaliana plants. In contrast to animal models, we find that Arabidopsis sp. suppresses Q69 aggregation through chloroplast proteostasis. Inhibition of chloroplast proteostasis diminishes the capacity of plants to prevent cytosolic Q69 aggregation. Moreover, endogenous polyQ-containing proteins also aggregate on chloroplast dysfunction. We find tha