First Records of Stelis permaculata Cockerell (Hymenoptera: Megachilidae) in Minnesota, United States of America and Manitoba, Canada

Abstract New records are reported for the cleptoparasitic bee Stelis permaculata Cockerell (Hymenoptera: Megachilidae) from Minnesota, United States of America and Manitoba, Canada. Minnesota records come from trap-nests, which also collected the host, Heriades carinata Cresson

Minnesota State Records for Osmia georgica, Megachile inimica, and Megachile frugalis (Hymenoptera, Megachilidae), Including a New Nest Description for Megachile frugalis Compared with Other Species in the Subgenus Sayapis

In this note, we report the first Minnesota state records of Osmia (Helicosmia) georgica Cresson 1878,Megachile (Sayapis) inimica Cresson 1872, and Megachile (Sayapis) frugalis Cresson 1872, which were collected in 2018. We also provide the first description of the nest structure of M. frugalis. All three species typically have more southern distributions. The nest of M. frugalis shows similar structure to other species in the subgenus Sayapis Titus, such as M. inimica and M. pugnata, particularly in that the longitudinal nest cell walls lack a lining of leaf pieces, and the cell partitions are made from a layer of leaf pieces followed by a layer of masticated vegetation and soil particles

Comprehensive mutational analysis of a cohort of Swedish Cornelia de Lange syndrome patients

Cornelia de Lange syndrome (CdLS; OMIM 122470) is a rare multiple congenital anomaly/mental retardation syndrome characterized by distinctive dysmorphic facial features, severe growth and developmental delay and abnormalities of the upper limbs. About 50% of CdLS patients have been found to have heterozygous mutations in the NIPBL gene and a few cases were recently found to be caused by mutations in the X-linked SMC1L1 gene. We performed a mutation screening of all NIPBL coding exons by direct sequencing in 11 patients ( nine sporadic and two familial cases) diagnosed with CdLS in Sweden and detected mutations in seven of the cases. All were de novo, and six of the mutations have not been previously described. Four patients without identifiable NIPBL mutations were subsequently subjected to multiplex ligation-dependent probe amplification analysis to exclude whole exon deletions/duplications of NIPBL. In addition, mutation analysis of the 50 untranslated region (5' UTR) of NIPBL was performed. Tiling resolution array comparative genomic hybridization analysis was carried out on these four patients to detect cryptic chromosome imbalances and in addition the boys were screened for SMC1L1 mutations. We found a de novo 9p duplication with a size of 0.6Mb in one of the patients with a CdLS-like phenotype but no mutations were detected in SMC1L1. So far, two genes ( NIPBL and SMC1L1) have been identified causing CdLS or CdLS-like phenotypes. However, in a considerable proportion of individuals demonstrating the CdLS phenotype, mutations in any of these two genes are not found and other potential loci harboring additional CdLS-causing genes should be considered