Weinstein, A. M. | bioRxiv Science

bioRxiv2022

Critical pollination chemistry: Specific sesquiterpene floral volatiles in carrot inhibit honey bee feeding.

O_LIAlthough many plant species are reliant on insect pollination, agricultural plant breeding programs have primarily focused on traits that appeal to growers and consumers, rather than on floral traits that enhance pollinator attraction. In some vegetable seed production systems, this has led to declining pollinator attraction and poor seed yields. C_LIO_LIWe predicted that low-yielding crop varieties would be less attractive to pollinators due to deficiencies in nectar rewards or volatile floral attractants. To test our prediction, we used a chemical phenotyping approach to examine how floral chemical traits of five carrot lines affect honey bee visitation. C_LIO_LIIn bioassays, honey bees avoided feeders containing nectar from all carrot lines indicating a general non-attractant effect. Certain compounds in carrot flowers and nectar not only failed to elicit attraction but functioned as repellents, including the sesquiterpenes -selinene and {beta}-selinene. Others enhanced attraction, e.g. {beta}-ocimene. C_LIO_LIThe repellent sesquiterpenes have previously been implicated in plant defense suggesting a fine balance between pollination and plant protection, which when disrupted in artificial selection in plant breeding programs can impact the crop yield. These new insights highlight the importance of bioactive compounds in attracting pollinators toward floral resources in both ecological and agricultural settings. C_LI

plant biology↗

bioRxiv2022

A mitochondrial blood-based patient stratification candidate biomarker for Parkinson's disease

Parkinsons disease (PD) is the most common neurodegenerative movement disorder and neuroprotective interventions remain elusive. High throughput biomarkers aimed to stratify patients based on shared etiology is one critical path to the success of disease-modifying therapies in clinical trials. Mitochondrial dysfunction plays a prominent role in the pathogenesis of PD. Previously, we found brain region-specific mitochondrial DNA (mtDNA) damage accumulation in neuronal and in vivo PD models, as well as human PD postmortem brain tissue. In this study, to investigate mtDNA damage as a potential blood biomarker for PD, we describe a novel Mito DNADX assay that allows for the accurate real-time quantification of mtDNA damage in a 96-well platform, compatible with assessing large cohorts of patient samples. We found that levels of mtDNA damage were increased in blood derived from early-stage idiopathic PD patients or those harboring the pathogenic LRRK2 G2019S mutation compared to age-matched healthy controls. Given that increased mtDNA damage was also found in non-manifesting LRRK2 mutation carriers, mtDNA damage may begin to accumulate prior to a clinical PD diagnosis. LRRK2 kinase inhibition mitigated mtDNA damage in idiopathic PD models and patient-derived cells. The latter observations further substantiate a mechanistic role for wild-type LRRK2 kinase activity in idiopathic PD and support mtDNA damage reversal as a suitable approach to slow PD-related pathology. In light of recent advances in the field of precision medicine, the analysis of mtDNA damage as a blood-based patient stratification biomarker should be included in future clinical trials. One Sentence SummaryBlood test identifies Parkinsons patients most likely to respond to mitochondria-targeted therapeutics facilitating a precision medicine approach.

neuroscience↗