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White pupae phenotype of tephritids is caused by parallel mutations of a MFS transporter.

ABSTRACT: Mass releases of sterilized male insects, in the frame of sterile insect technique programs, have helped suppress insect pest populations since the 1950s. In the major horticultural pests Bactrocera dorsalis, Ceratitis capitata, and Zeugodacus cucurbitae, a key phenotype white pupae (wp) has been used for decades to selectively remove females before releases, yet the gene responsible remained unknown. Here, we use classical and modern genetic approaches to identify and functionally characterize causal wp^- mutations in these distantly related fruit fly species. We find that the wp phenotype is produced by parallel mutations in a single, conserved gene. CRISPR/Cas9-mediated knockout of the wp gene leads to the rapid generation of white pupae strains in C. capitata and B. tryoni. The conserved phenotype and independent nature of wp^- mutations suggest this technique can provide a generic approach to produce sexing strains in other major medical and agricultural insect pests.

SUBMITTER: Ward CM

PROVIDER: S-EPMC7820335 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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White pupae phenotype of tephritids is caused by parallel mutations of a MFS transporter.

Ward Christopher M CM Aumann Roswitha A RA Whitehead Mark A MA Nikolouli Katerina K Leveque Gary G Gouvi Georgia G Fung Elisabeth E Reiling Sarah J SJ Djambazian Haig H Hughes Margaret A MA Whiteford Sam S Caceres-Barrios Carlos C Nguyen Thu N M TNM Choo Amanda A Crisp Peter P Sim Sheina B SB Geib Scott M SM Marec František F Häcker Irina I Ragoussis Jiannis J Darby Alistair C AC Bourtzis Kostas K Baxter Simon W SW Schetelig Marc F MF

Nature communications 20210121 1

Mass releases of sterilized male insects, in the frame of sterile insect technique programs, have helped suppress insect pest populations since the 1950s. In the major horticultural pests Bactrocera dorsalis, Ceratitis capitata, and Zeugodacus cucurbitae, a key phenotype white pupae (wp) has been used for decades to selectively remove females before releases, yet the gene responsible remained unknown. Here, we use classical and modern genetic approaches to identify and functionally characterize ...[more]

PMID: 33479218

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Project description:Childhood onset motor neuron diseases or neuronopathies are a clinically heterogeneous group of disorders. A particularly severe subgroup first described in 1894, and subsequently called Brown-Vialetto-Van Laere syndrome, is characterized by progressive pontobulbar palsy, sensorineural hearing loss and respiratory insufficiency. There has been no treatment for this progressive neurodegenerative disorder, which leads to respiratory failure and usually death during childhood. We recently reported the identification of SLC52A2, encoding riboflavin transporter RFVT2, as a new causative gene for Brown-Vialetto-Van Laere syndrome. We used both exome and Sanger sequencing to identify SLC52A2 mutations in patients presenting with cranial neuropathies and sensorimotor neuropathy with or without respiratory insufficiency. We undertook clinical, neurophysiological and biochemical characterization of patients with mutations in SLC52A2, functionally analysed the most prevalent mutations and initiated a regimen of high-dose oral riboflavin. We identified 18 patients from 13 families with compound heterozygous or homozygous mutations in SLC52A2. Affected individuals share a core phenotype of rapidly progressive axonal sensorimotor neuropathy (manifesting with sensory ataxia, severe weakness of the upper limbs and axial muscles with distinctly preserved strength of the lower limbs), hearing loss, optic atrophy and respiratory insufficiency. We demonstrate that SLC52A2 mutations cause reduced riboflavin uptake and reduced riboflavin transporter protein expression, and we report the response to high-dose oral riboflavin therapy in patients with SLC52A2 mutations, including significant and sustained clinical and biochemical improvements in two patients and preliminary clinical response data in 13 patients with associated biochemical improvements in 10 patients. The clinical and biochemical responses of this SLC52A2-specific cohort suggest that riboflavin supplementation can ameliorate the progression of this neurodegenerative condition, particularly when initiated soon after the onset of symptoms.

Dataset Information

White pupae phenotype of tephritids is caused by parallel mutations of a MFS transporter.

Publications

White pupae phenotype of tephritids is caused by parallel mutations of a MFS transporter.

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