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At least 955 records · Page 53

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NASA NTRS2002

Gene conversion is strongly induced in human cells by double-strand breaks and is modulated by the expression of BCL-x(L)

Homology-directed repair (HDR) of DNA double-strand breaks (DSBs) contributes to the maintenance of genomic stability in rodent cells, and it has been assumed that HDR is of similar importance in DSB repair in human cells. However, some outcomes of homologous recombination can be deleterious, suggesting that factors exist to regulate HDR. We demonstrated previously that overexpression of BCL-2 or BCL-x(L) enhanced the frequency of X-ray-induced TK1 mutations, including loss of heterozygosity events presumed to arise by mitotic recombination. The present study was designed to test whether HDR is a prominent DSB repair pathway in human cells and to determine whether ectopic expression of BCL-x(L) affects HDR. Using TK6-neo cells, we find that a single DSB in an integrated HDR reporter stimulates gene conversion 40-50-fold, demonstrating efficient DSB repair by gene conversion in human cells. Significantly, DSB-induced gene conversion events are 3-4-fold more frequent in TK6 cells that stably overexpress the antiapoptotic protein BCL-X(L). Thus, HDR plays an important role in maintaining genomic integrity in human cells, and ectopic expression of BCL-x(L) enhances HDR of DSBs. This is the first study to highlight a function for BCL-x(L) in modulating DSB repair in human cells.

NASA Discipline Radiation Health↗

NASA NTRS2000

Ionizing-radiation resistance in the desiccation-tolerant cyanobacterium Chroococcidiopsis

The effect of X-ray irradiation on cell survival, induction, and repair of DNA damage was studied by using 10 Chroococcidiopsis strains isolated from desert and hypersaline environments. After exposure to 2.5 kGy, the percentages of survival for the strains ranged from 80 to 35%. In the four most resistant strains, the levels of survival were reduced by 1 or 2 orders of magnitude after irradiation with 5 kGy; viable cells were recovered after exposure to 15 kGy but not after exposure to 20 kGy. The severe DNA damage evident after exposure to 2.5 kGy was repaired within 3 h, and the severe DNA damage evident after exposure to 5 kGy was repaired within 24 h. The increase in trichloroacetic acid-precipitable radioactivity in the culture supernatant after irradiation with 2.5 kGy might have been due to cell lysis and/or an excision process involved in DNA repair. The radiation resistance of Chroococcidiopsis strains may reflect the ability of these cyanobacteria to survive prolonged desiccation through efficient repair of the DNA damage that accumulates during dehydration.

Non-NASA Center↗

DOE OSTI2018

The Pleckstrin homology like domain family member, TDAG51, is temporally regulated during skeletal muscle regeneration

Highlights: • TDAG51 expression is low but detectable in undamaged skeletal muscle. • Muscle expression of TDAG51 increases significantly in response to damage and insulin-like growth factor 1 (IGF-1). • Mice lacking TDAG51 display reduced functional capacity and a delay in the early regenerative phases of muscle repair. • Despite early delays in regeneration, TDAG51null mice can compensate and normalize muscle repair by 10 days post injury. The capacity for skeletal muscle to repair from daily insults as well as larger injuries is a vital component to maintaining muscle health over our lifetime. Given the importance of skeletal muscle for our physical and metabolic well-being, identifying novel factors mediating the growth and repair of skeletal muscle will thus build our foundational knowledge and help lead to potential therapeutic avenues for muscle wasting disorders. To that end, we investigated the expression of T-cell death associated gene 51 (TDAG51) during skeletal muscle repair and studied the response of TDAG51 deficient (TDAG51{sup -/-}) mice to chemically-induced muscle damage. TDAG51 mRNA and protein expression within uninjured skeletal muscle is almost undetectable but, in response to chemically-induced muscle damage, protein levels increase by 5 days post-injury and remain elevated for up to 10 days of regeneration. To determine the impact of TDAG51 deletion on skeletal muscle form and function, we compared adult male TDAG51{sup -/-} mice with age-matched wild-type (WT) mice. Body and muscle mass were not different between the two groups, however, in situ muscle testing demonstrated a significant reduction in force production both before and after fatiguing contractions in TDAG51{sup -/-} mice. During the early phases of the regenerative process (5 days post-injury), TDAG51{sup -/-} muscles display a significantly larger area of degenerating muscle tissue concomitant with significantly less regenerating area compared to WT (as demonstrated by embryonic myosin heavy chain expression). Despite these early deficits in regeneration, TDAG51{sup -/-} muscles displayed no morphological deficits by 10 days post injury compared to WT mice. Taken together, the data presented herein demonstrate TDAG51 expression to be upregulated in damaged skeletal muscle and its absence attenuates the early phases of muscle regeneration.

60 APPLIED LIFE SCIENCES↗

DOE OSTI2022

Cas9-induced large deletions and small indels are controlled in a convergent fashion

Repair of Cas9-induced double-stranded breaks results primarily in formation of small insertions and deletions (indels), but can also cause potentially harmful large deletions. While mechanisms leading to the creation of small indels are relatively well understood, very little is known about the origins of large deletions. Using a library of clonal NGS-validated mouse embryonic stem cells deficient for 32 DNA repair genes, we have shown that large deletion frequency increases in cells impaired for non-homologous end joining and decreases in cells deficient for the central resection gene Nbn and the microhomology-mediated end joining gene Polq. Across deficient clones, increase in large deletion frequency was closely correlated with the increase in the extent of microhomology and the size of small indels, implying a continuity of repair processes across different genomic scales. Furthermore, by targeting diverse genomic sites, we identified examples of repair processes that were highly locus-specific, discovering a role for exonuclease Trex1. Finally, we present evidence that indel sizes increase with the overall efficiency of Cas9 mutagenesis. These findings may have impact on both basic research and clinical use of CRISPR-Cas9, in particular in conjunction with repair pathway modulation.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2024

DNA double-strand break movement in heterochromatin depends on the histone acetyltransferase dGcn5

Abstract Cells employ diverse strategies to repair double-strand breaks (DSBs), a dangerous form of DNA damage that threatens genome integrity. Eukaryotic nuclei consist of different chromatin environments, each displaying distinct molecular and biophysical properties that can significantly influence the DSB-repair process. DSBs arising in the compact and silenced heterochromatin domains have been found to move to the heterochromatin periphery in mouse and Drosophila to prevent aberrant recombination events. However, it is poorly understood how chromatin components, such as histone post-translational modifications, contribute to these DSB movements within heterochromatin. Using irradiation as well as locus-specific DSB induction in Drosophila tissues and cultured cells, we find enrichment of histone H3 lysine 9 acetylation (H3K9ac) at DSBs in heterochromatin but not euchromatin. We find this increase is mediated by the histone acetyltransferase dGcn5, which rapidly localizes to heterochromatic DSBs. Moreover, we demonstrate that in the absence of dGcn5, heterochromatic DSBs display impaired recruitment of the SUMO E3 ligase Nse2/Qjt and fail to relocate to the heterochromatin periphery to complete repair. In summary, our results reveal a previously unidentified role for dGcn5 and H3K9ac in heterochromatic DSB repair and underscore the importance of differential chromatin responses at heterochromatic and euchromatic DSBs to promote safe repair.

Biochemistry & Molecular Biology↗

DOE OSTI2013

Structure of human apurinic/apyrimidinic endonuclease 1 with the essential Mg 2+ cofactor

Apurinic/apyrimidinic endonuclease 1 (APE1) mediates the repair of abasic sites and other DNA lesions and is essential for base-excision repair and strand-break repair pathways. APE1 hydrolyzes the phosphodiester bond at abasic sites, producing 5'-deoxyribose phosphate and the 3'-OH primer needed for repair synthesis. It also has additional repair activities, including the removal of 3'-blocking groups. APE1 is a powerful enzyme that absolutely requires Mg 2+ , but the stoichiometry and catalytic function of the divalent cation remain unresolved for APE1 and for other enzymes in the DNase I superfamily. Previously reported structures of DNA-free APE1 contained either Sm 3+ or Pb 2+ in the active site. However, these are poor surrogates for Mg 2+ because Sm 3+ is not a cofactor and Pb 2+ inhibits APE1, and their coordination geometry is expected to differ from that of Mg 2+ . A crystal structure of human APE1 was solved at 1.92 Å resolution with a single Mg 2+ ion in the active site. The structure reveals ideal octahedral coordination of Mg 2+ via two carboxylate groups and four water molecules. One residue that coordinates Mg 2+ directly and two that bind inner-sphere water molecules are strictly conserved in the DNase I superfamily. This structure, together with a recent structure of the enzyme–product complex, inform on the stoichiometry and the role of Mg 2+ in APE1-catalyzed reactions.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2021

Genomic reconstruction of fossil and living microorganisms in ancient Siberian permafrost

Abstract Background Total DNA (intracellular, iDNA and extracellular, eDNA) from ancient permafrost records the mixed genetic repository of the past and present microbial populations through geological time. Given the exceptional preservation of eDNA under perennial frozen conditions, typical metagenomic sequencing of total DNA precludes the discrimination between fossil and living microorganisms in ancient cryogenic environments. DNA repair protocols were combined with high throughput sequencing (HTS) of separate iDNA and eDNA fraction to reconstruct metagenome-assembled genomes (MAGs) from ancient microbial DNA entrapped in Siberian coastal permafrost. Results Despite the severe DNA damage in ancient permafrost, the coupling of DNA repair and HTS resulted in a total of 52 MAGs from sediments across a chronosequence (26–120 kyr). These MAGs were compared with those derived from the same samples but without utilizing DNA repair protocols. The MAGs from the youngest stratum showed minimal DNA damage and thus likely originated from viable, active microbial species. Many MAGs from the older and deeper sediment appear related to past aerobic microbial populations that had died upon freezing. MAGs from anaerobic lineages, including Asgard archaea, however exhibited minimal DNA damage and likely represent extant living microorganisms that have become adapted to the cryogenic and anoxic environments. The integration of aspartic acid racemization modeling and metaproteomics further constrained the metabolic status of the living microbial populations. Collectively, combining DNA repair protocols with HTS unveiled the adaptive strategies of microbes to long-term survivability in ancient permafrost. Conclusions Our results indicated that coupling of DNA repair protocols with simultaneous sequencing of iDNA and eDNA fractions enabled the assembly of MAGs from past and living microorganisms in ancient permafrost. The genomic reconstruction from the past and extant microbial populations expanded our understanding about the microbial successions and biogeochemical alterations from the past paleoenvironment to the present-day frozen state. Furthermore, we provided genomic insights into long-term survival mechanisms of microorganisms under cryogenic conditions through geological time. The combined strategies in this study can be extrapolated to examine other ancient non-permafrost environments and constrain the search for past and extant extraterrestrial life in permafrost and ice deposits on Mars.

54 ENVIRONMENTAL SCIENCES↗

DOE OSTI2015

Progerin, the protein responsible for the Hutchinson-Gilford progeria syndrome, increases the unrepaired DNA damages following exposure to ionizing radiation

Introduction: Progerin, the protein responsible for the Hutchinson-Gilford Progeria Syndrome (HGPS), is a partially deleted form of nuclear lamin A, and its expression has been suggested as a cause for dysfunctional nuclear membrane and premature senescence. To examine the role of nuclear envelop architecture in regulating cellular aging and DNA repair, we used ionizing radiation to increase the number of DNA double strand breaks (DSBs) in normal and HGPS cells, and analyzed possible relationship between unrepaired DSBs and cellular aging. Results: We found that HGPS cells are normal in repairing a major fraction of radiation-induced double strand breaks (M-DSBs)but abnormal to show increased amount of residual unrepaired DSBs (R-DSBs). Such unrepaired DSBs were 2.6 times (CI 95 %: 2.2–3.2) higher than that in normal cells one week after the irradiation, and 1.6 times (CI 95 %: 1.3–1.9) higher even one month after the irradiation. These damages tend to increase as the nuclear envelope become abnormal, a characteristic of both HGPS and normal human cells which undergo replicative senescence. The artificial, enforced over-expression of progerin further impaired the repair of M-DSBs, implying lamin A-associated nuclear membrane has an important role for DNA DSB repair. Introduction of telomerase gene function in HGPS cells reversed such aging phenotypes along with upregulation of lamin B1 and downregulation of progerin, which is a hallmark of young cells. Conclusion: We suggest that lamin A- or progerin-associated nuclear envelope is involved in cellular aging associated with DNA damage repair.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2014

Combinatorial DNA Damage Pairing Model Based on X-Ray-Induced Foci Predicts the Dose and LET Dependence of Cell Death in Human Breast Cells

In contrast to the classic view of static DNA double-strand breaks (DSBs) being repaired at the site of damage, we hypothesize that DSBs move and merge with each other over large distances (m). As X-ray dose increases, the probability of having DSB clusters increases as does the probability of misrepair and cell death. Experimental work characterizing the X-ray dose dependence of radiation-induced foci (RIF) in nonmalignant human mammary epithelial cells (MCF10A) is used here to validate a DSB clustering model. We then use the principles of the local effect model (LEM) to predict the yield of DSBs at the submicron level. Two mechanisms for DSB clustering, namely random coalescence of DSBs versus active movement of DSBs into repair domains are compared and tested. Simulations that best predicted both RIF dose dependence and cell survival after X-ray irradiation favored the repair domain hypothesis, suggesting the nucleus is divided into an array of regularly spaced repair domains of ~;;1.55 m sides. Applying the same approach to high-linear energy transfer (LET) ion tracks, we are able to predict experimental RIF/m along tracks with an overall relative error of 12percent, for LET ranging between 30 350 keV/m and for three different ions. Finally, cell death was predicted by assuming an exponential dependence on the total number of DSBs and of all possible combinations of paired DSBs within each simulated RIF. Relative biological effectiveness (RBE) predictions for cell survival of MCF10A exposed to high-LET showed an LET dependence that matches previous experimental results for similar cell types. Overall, this work suggests that microdosimetric properties of ion tracks at the submicron level are sufficient to explain both RIF data and survival curves for any LET, similarly to the LEM assumption. Conversely, high-LET death mechanism does not have to infer linear-quadratic dose formalism as done in the LEM. In addition, the size of repair domains derived in our model are based on experimental RIF and are three times larger than the hypothetical LEM voxel used to fit survival curves. Our model is therefore an alternative to previous approaches that provides a testable biological mechanism (i.e., RIF). In addition, we propose that DSB pairing will help develop more accurate alternatives to the linear cancer risk model (LNT) currently used for regulating exposure to very low levels of ionizing radiation.

59 BASIC BIOLOGICAL SCIENCES↗

DOE OSTI2018

Persistence of Gamma-H2AX Foci in Bronchial Cells Correlates with Susceptibility to Radiation Associated Lung Cancer in Mice

The risk of developing radiation-induced lung cancer differs between different strains of mice, but the underlying cause of the strain differences is unknown. Strains of mice also differ in how quickly they repair radiation-induced DNA double-strand breaks (DSBs). We assayed mouse strains from the CcS/Dem recombinant congenic strain set for their efficacy in repairing DNA DSBs during protracted irradiation. We measured unrepaired γ-H2AX radiation-induced foci (RIF), which persisted after chronic 24-h gamma irradiation, as a surrogate marker for repair efficiency in bronchial epithelial cells for 17 of the CcS/Dem strains and the BALB/c founder strain. We observed a very strong correlation (R2 = 79.18%, P < 0.001) between the level of unrepaired RIF and radiogenic lung cancer incidence measured in the same strains. Interestingly, spontaneous levels of foci in nonirradiated mice also showed good correlation with lung cancer incidence when incidence data from male and female mice were combined. These results suggest that genetic differences in DNA repair capacity largely account for differing susceptibilities to radiationinduced lung cancer among CcS/Dem mouse strains, and that high levels of spontaneous DNA damage are also a relatively good marker of cancer predisposition. In a smaller pilot study, we found that the repair capacity measured in peripheral blood leucocytes also correlated well with radiogenic lung cancer susceptibility, raising the possibility that the assay could be used to detect radiogenic lung cancer susceptibility in humans.

60 APPLIED LIFE SCIENCES↗

NASA NTRS1975

Statistical estimation of service cracks and maintenance cost for aircraft structures

A method is developed for the statistical estimation of the number of cracks to be repaired in service as well as the repair and the maintenance costs. The present approach accounts for the statistical distribution of the initial crack size, the statistical nature of the NDI technique used for detecting the crack, and the renewal process for the crack propagation of repaired cracks. The mean and the standard deviation of the cumulative number of cracks to be repaired are computed as a function of service time. The statistics of the costs of repair and maintenance, expressed in terms of the percentage of the cost of replacement, are estimated as a function of service time. The results of the present study provide relevant information for the decision of fleet management, the estimation of life cycle cost, and procurement specifications. The present study is essential to the design and cost optimization of aircraft structures.

Yang, J.-N.↗

NASA NTRS1992

Effect of spaceflight on the extracellular matrix of skeletal muscle after a crush injury

The organization and composition of the extracellular matrix were studied in the crush-injured gastrocnemius muscle of rats subjected to 0 G. After 14 days of flight on Cosmos 2044, the gastrocnemius muscle was removed and evaluated by histochemical and immunohistochemical techniques from the five injured flight rodents and various earth-based treatment groups. In general, the repair process was similar in all injured muscle samples with regard to the organization of the extracellular matrix and myofibers. Small and large myofibers were present within an expanded extracellular matrix, indicative of myogenesis and muscle regeneration. In the tail-suspended animals, a more complete repair was observed with nonenlarged area of nonmuscle cells or matrix material visible. In contrast, the muscle samples from the flight animals were less well organized and contained more macrophages and blood vessels in the repair region, indicative of a delayed repair process, but did not demonstrate any chronic inflammation. Myofiber repair did vary in muscles from the different groups, being slowest in the flight animals and most complete in the tail-suspended ones.

Stauber, W. T.↗

NASA NTRS1996

Ames Research Center Shear Tests of SLA-561V Heat Shield Material for Mars-Pathfinder

This report describes the results of arc-jet testing at Ames Research Center on behalf of Jet Propulsion Laboratory (JPL) for the development of the Mars-Pathfinder heat shield. The current test series evaluated the performance of the ablating SLA-561V heat shield material under shear conditions. In addition, the effectiveness of several methods of repairing damage to the heat shield were evaluated. A total of 26 tests were performed in March 1994 in the 2 in. X 9 in. arc-heated turbulent Duct Facility, including runs to calibrate the facility to obtain the desired shear stress conditions. A total of eleven models were tested. Three different conditions of shear and heating were used. The non-ablating surface shear stresses and the corresponding, approximate, non-ablating surface heating rates were as follows: Condition 1, 170 N/m(exp 2) and 22 W/cm(exp 2); Condition 2, 240 N/m(exp 2) and 40 W/cm(exp 2); Condition 3, 390 N/m(exp 2) and 51 W/cm(exp 2). The peak shear stress encountered in flight is represented approximately by Condition 1; however, the heating rate was much less than the peak flight value. The peak heating rate that was available in the facility (at Condition 3) was about 30 percent less than the maximum value encountered during flight. Seven standard ablation models were tested, of which three models were instrumented with thermocouples to obtain in-depth temperature profiles and temperature contours. An additional four models contained a variety of repair plugs, gaps, and seams. These models were used to evaluated different repair materials and techniques, and the effect of gaps and construction seams. Mass loss and surface recession measurements were made on all models. The models were visually inspected and photographed before and after each test. The SLA-561 V performed well; even at test Condition 3, the char remained intact. Most of the resins used for repairs and gap fillers performed poorly. However, repair plugs made of SLA-561V performed well. Approximately 70 percent of the thermocouples yielded good data.

Tauber, Michael↗

NASA NTRS1997

2195 Aluminum-Copper-Lithium Friction Plug Welding Development

Technology developments and applications of friction plug welding is presented. This friction repair welding technology is being studied for implementation on the Space Transportation System's Super Light Weight External Tank. Single plug repairs will be used on a vast majority of weld defects, however, linear defects of up to several inches can be repaired by overlapping plug welds. Methods and results of tensile, bend, simulated service, surface crack tension and other tests at room and cryogenic temperatures is discussed. Attempts to implement Friction Plug Welding has led to both tool and process changes in an attempt to minimize expansive tooling and lengthy implementation times. Process control equipment and data storage methods intended for large scale production will also be addressed. Benefits include increased strength and toughness, decreased weld repair time, automated and highly reliable process, and a lower probability of having to re-repair defect locations.

Takeshita, Rike P.↗

NASA NTRS2000

Homologous recombination as a potential target for caffeine radiosensitization in mammalian cells: reduced caffeine radiosensitization in XRCC2 and XRCC3 mutants

The radiosensitizing effect of caffeine has been associated with the disruption of multiple DNA damage-responsive cell cycle checkpoints, but several lines of evidence also implicate inhibition of DNA repair. The role of DNA repair inhibition in caffeine radiosensitization remains uncharacterized, and it is unknown which repair process, or lesion, is affected. We show that a radiosensitive cell line, mutant for the RAD51 homolog XRCC2 and defective in homologous recombination repair (HRR), displays significantly diminished caffeine radiosensitization that can be restored by expression of XRCC2. Despite the reduced radiosensitization, caffeine effectively abrogates checkpoints in S and G2 phases in XRCC2 mutant cells indicating that checkpoint abrogation is not sufficient for radiosensitization. Another radiosensitive line, mutant for XRCC3 and defective in HRR, similarly shows reduced caffeine radiosensitization. On the other hand, a radiosensitive mutant (irs-20) of DNA-PKcs with a defect in non-homologous end-joining (NHEJ) is radiosensitized by caffeine to an extent comparable to wild-type cells. In addition, rejoining of radiation-induced DNA DSBs, that mainly reflects NHEJ, remains unaffected by caffeine in XRCC2 and XRCC3 mutants, or their wild-type counterparts. These observations suggest that caffeine targets steps in HRR but not in NHEJ and that abrogation of checkpoint response is not sufficient to explain radiosensitization. Indeed, immortalized fibroblasts from AT patients show caffeine radiosensitization despite the checkpoint defects associated with ATM mutation. We propose that caffeine radiosensitization is mediated by inhibition of stages in DNA DSB repair requiring HRR and that checkpoint disruption contributes by allowing these DSBs to transit into irreparable states. Thus, checkpoints may contribute to genomic stability by promoting error-free HRR.

NASA Discipline Radiation Health↗

NASA NTRS2005

Return to Flight Resource Reel 1 of 2

A video presentation detailing the tests performed on the Space Shuttle Discovery in preparation for its return to flight is shown. The tests include: 1) Reinforced Carbon-Carbon (RCC) Impact Test Article; 2) RCC Foam Impact Testing; 3) Thermal Protection System (TPS) Ice Impact Testing featuring Justin Kerr, Project Engineer; 4) Wing Leading Edge Wireless Sensors featuring Karl Kiefer, President and CEO of Invocon, and Kevin Champaigne of Invocon; 5) TPS Repair Testing KC-135 Zero-G Environment featuring Soichi Noguchi, Mission Specialist; 6) TPS Extravehicular Activity Tool Demonstration; 7) TPS Repair Testing Vacuum Glove box; 8) TPS Repair Testing Human Thermal Vacuum Chamber; 9) TPS Reentry Testing Atmospheric Reentry Materials and Structures Evaluation Facility; 10) TPS Alternative Repair Concept; 11) Lora Bailey Lead Engineer for EVA Tools; 12) Reinforced Carbon-Carbon ATK Thiokol Plug Repair Animation; 13) 3-Percent Model Build-Up; and 14) Wind Tunnel Testing RCC Aging Research Ballistic Testing.

Source record↗

NASA NTRS2004

The Effects of Modeled Microgravity on Nucleocytoplasmic Localization of Human Apurinic/Apyrimidinic

Exposure to space radiation and microgravity occurs to humans during space flight. In order to have accurate risk estimations, answering questions to whether increased DNA damage seen during space flight in modified by microgravity are important. Several studies have examined whether intercellular repair of radiation-induced DNA lesions are modified by microgravity. Results from these studies show no modification of the repair processes due to microgravity. However, it is known that in studies not involving radiation that microgravity interferes with normal development. Interestingly, there is no data that attempts to analyze the possible effects of microgravity on the trafficking of DNA repair proteins. In this study, we analyze the effects of modeled microgravity on nucleocytoplasmic shuttling of the human DNA repair enzyme apurinic/apyrimidinic endonuclease 1 (APE1/Ref1) which is involved in base excision repair. We examined nuclear translocation of APE1 using enhanced green fluorescent protein (EGFP) fused to APE1 as a reporter. While APE1 under normal gravity showed normal nuclear localization, APE1 nuclear localization under modeled microgravity was decreased. These results suggest that nucleocytoplasmic translocation of APE1 is modified under modeled microgravity.

Gonda, Steve↗

NASA NTRS2012

Soldering in a Reduced Gravity Environment (SoRGE)

Future long-duration human exploration missions will be challenged by constraints on mass and volume allocations available for spare parts. Addressing this challenge will be critical to the success of these missions. As a result, it is necessary to consider new approaches to spacecraft maintenance and repair that reduce the need for large replacement components. Currently, crew members on the International Space Station (ISS) recover from faults by removing and replacing, using backup systems, or living without the function of Orbital Replacement Units (ORUs). These ORUs are returned to a depot where the root cause of the failure is determined and the ORU is repaired. The crew has some limited repair capability with the Modulation/DeModulation (MDM) ORU, where circuit cards are removed and replace in faulty units. The next step to reducing the size of the items being replaced would be to implement component-level repair. This mode of repair has been implemented by the U.S. Navy in an operational environment and is now part of their standard approach for maintenance. It is appropriate to consider whether this approach can be adapted for future spaceflight operations. To this end, the Soldering in a Reduced Gravity Environment (SoRGE) experiment studied the effect of gravity on the formation of solder joints on electronic circuit boards. This document describes the SoRGE experiment, the analysis methods, and results to date. This document will also contain comments from the crew regarding their experience conducting the SoRGE experiment as well as recommendations for future improvements. Finally, this document will discuss the plans for the SoRGE samples which remain on ISS.

Easton, John W.↗