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Biology subjects

Maas, R.

Publications and source records attributed to Maas, R..

2 recordsLinked to original sources

How much pollen do solitary bee larvae consume? Or establishing realistic exposure estimates of solitary bee larvae via pollen for the use in risk assessment

Bees foraging in agricultural habitats can be exposed to plant protection products. In order to limit the risk of adverse events to occur a robust risk assessment is needed, which requires reliable estimates for the expected exposure. Especially the exposure pathways to developing solitary bees are not well described and in the currently proposed form rely on limited information. To address this topic, we used a published data set on the volume of pollen solitary bees provide for their larvae to build two scaling models predicting the amount of protein and pollen developing solitary bees need based on adult body weight. We test our models using both literature and experimental data, which both support the validity of the presented models. Using scaling models in the bee risk assessment could complement existing risk assessment approaches, facilitate the further development of accurate risk characterization for solitary bees and ultimately will help to protect them during their foraging activity in agricultural settings.

ecology↗

ALX1-related Frontonasal Dysplasia Results From Defective Neural Crest Cell Development and Migration

A pedigree of subjects with frontonasal dysplasia (FND) presented with bilateral oblique facial clefts and ocular phenotypes. Genome sequencing and analysis identified a L165F missense variant in the homeodomain of the transcription factor ALX1 which was imputed to be pathogenic. Induced pluripotent stem cells (iPSC) were derived from the subjects and differentiated to neural crest cells (NCC). NCC derived from ALX1L165F/L165F iPSC were more sensitive to apoptosis, showed an elevated expression of several neural crest progenitor state markers, and exhibited impaired migration compared to wild type controls. NCC migration was also evaluated in vivo using lineage tracing in a zebrafish model, which revealed defective migration of the anterior NCC stream that contributes to the median portion of the anterior neurocranium, phenocopying the clinical presentation. Analysis of human NCC culture media revealed a change in the level of bone morphogenic proteins (BMP), with a low-level of BMP2 and a high level of BMP9. Soluble BMP2 and BMP9 antagonist treatments were able to rescue the defective migration phenotype. Taken together, these results demonstrate a mechanistic requirement of ALX1 in NCC development and migration.

cell biology↗