Key result
SGCB p.Thr182Pro variant links to specific marker haplotypes in ~85% of Indian LGMD patients.
Why the study?
To summarize molecularly diagnosed LGMD cases and understand the genetic structure of patients carrying the recurrent SGCB p.Thr182Pro variant.
Observational (n=1,046)
Absolute Event Rate: 85.3% vs 0%
The study identifies a shared ~1 Mb region of homozygosity and founder effect for the SGCB p.Thr182Pro variant in Indian patients with limb-girdle muscular dystrophy.
May guide targeted screening in Indian LGMD; leaves open validation of haplotype-based diagnostics.
The sarcoglycanopathies are autosomal recessive limb-girdle muscular dystrophies (LGMDs) caused by the mutations in genes encoding the α, β, γ, and δ proteins which stabilizes the sarcolemma of muscle cells. The clinical phenotype is characterized by progressive proximal muscle weakness with childhood onset. Muscle biopsy findings are diagnostic in confirming dystrophic changes and deficiency of one or more sarcoglycan proteins. In this study, we summarized 1,046 LGMD patients for which a precise diagnosis was identified using targeted sequencing. The most frequent phenotypes identified in the patients are LGMDR1 (19.7%), LGMDR4 (19.0%), LGMDR2 (17.5%), and MMD1 (14.5%). Among the reported genes, each of CAPN3, SGCB, and DYSF variants was reported in more than 10% of our study cohort. The most common variant SGCB p.Thr182Pro was identified in 146 (12.5%) of the LGMD patients, and in 97.9% of these patients, the variant was found to be homozygous. To understand the genetic structure of the patients carrying SGCB p.Thr182Pro, we genotyped 68 LGMD patients using a whole genome microarray. Analysis of the array data identified a large ~1 Mb region of homozygosity (ROH) (chr4:51817441-528499552) suggestive of a shared genomic region overlapping the recurrent missense variant and shared across all 68 patients. Haplotype analysis identified 133 marker haplotypes that were present in ~85.3% of the probands as a double allele and absent in all random controls. We also identified 5 markers (rs1910739, rs6852236, rs13122418, rs13353646, and rs6554360) which were present in a significantly higher proportion in the patients compared to random control set ( n = 128 ) and the population database. Of note, admixture analysis was suggestive of greater proportion of West Eurasian/European ancestry as compared to random controls. Haplotype analysis and frequency in the population database indicate a probable event of founder effect. Further systematic study is needed to identify the communities and regions where the SGCB p.Thr182Pro variant is observed in higher proportions. After identifying these communities and//or region, a screening program is needed to identify carriers and provide them counselling.
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Manjunath et al. (2023) conducted an observational in Autosomal recessive limb-girdle muscular dystrophy (n=1,046). SGCB p.Thr182Pro variant vs. Random controls was evaluated on Presence of 133 marker haplotypes as a double allele. The SGCB p.Thr182Pro variant in Indian LGMD patients was associated with a ~1 Mb region of homozygosity, with specific marker haplotypes present in 85.3% of probands and absent in controls.
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