Phylogeography of the planktonic shrimp Lucifer hanseni Nobili 1905 in the Indo-Malayan Archipelago

Using partial sequences of two mitochondrial genes, cytochrome c oxidase subunit I (COI) and 12S ribosomal RNA (12S rRNA), and one nuclear gene, 28S ribosomal RNA (28S rRNA), we investigated population genetics of the holoplanktonic shrimp Lucifer hanseni Nobili, 1905 in the Indo-Malayan Archipelago (IMA), encompassing Andaman Sea, Malacca Strait, Gulf of Thailand, Borneo Island, Philippines (hereafter collectively referred to as the Thailand-Malaysia-Philippine area: TMP), Celebes Sea (CS), and the waters near islands in the Western Pacific (WP) including Palau, Papua New Guinea and Solomon Islands. The samples from the TMP showed the highest number of haplotypes. Significant phylogeographic structure was found in the L. hanseni populations (ΦST = 0.832 for COI, 0.159 for 12S rRNA, 0.783 for 28S rRNA). The total number of haplotypes was 46 in COI, 28 in 12S rRNA and 23 in 28S rRNA. The haplotype network analyses revealed two major clades for COI (subgroups: TMP + CS, WP) and for 12S rRNA and 28S rRNA (TMP, CS + WP). The CS and WP populations appeared isolated from the TMP populations. The samples from the CS showed low genetic diversity compared with the other samples at both haplotype and nucleotide levels, suggesting that the population CS experienced bottleneck events. This is the first demonstration of significant genetic structure of a holoplanktonic metazoan in IMA, which is suggested to be synergistically influenced by historical events (vicariance) and contemporary oceanographic circulations and corroborates the results of previous studies on other benthic/demersal animals with mero-planktonic phases

Data supporting mitochondrial morphological changes by SPG13-associated HSPD1 mutants

The data is related to the research article entitled “Hypomyelinating leukodystrophy-associated missense mutation in HSPD1 blunts mitochondrial dynamics” [1]. In addition to hypomyelinating leukodystrophy (HLD) 4 (OMIM no. 612233), it is known that spastic paraplegia (SPG) 13 (OMIM no. 605280) is caused by HSPD1’s amino acid mutation. Two amino acid mutations Val-98-to-Ile (V98I) and Gln-461-to-Glu (Q461E) are associated with SPG13 [2]. In order to investigate the effects of HSPD1’s V98I or Q461E mutant on mitochondrial morphological changes, we transfected each of the respective mutant-encoding genes into Cos-7 cells. Either of V98I or Q461E mutant exhibited increased number of mitochondria and short length mitochondrial morphologies. Using MitoTracker dye-incorporating assay, decreased mitochondrial membrane potential was also observed in both cases. The data described here supports that SPG13-associated HSPD1 mutant participates in causing aberrant mitochondrial morphological changes with decreased activities. Keywords: SPG13, HSPD1, Mitochondrion, Morphological chang

Data on the effect of hypomyelinating leukodystrophy 6 (HLD6)-associated mutations on the TUBB4A properties

Hypomyelinating leukodystrophy (HLD) is genetic demyelinating or dysmyelinating disease and is associated with at least 13 responsible genes. The mutations seem likely cause the functional deficiency of their gene products. HLD4- and HLD5-associated HSPD1 and FAM126A mutations affect biochemical properties of the gene products (Miyamoto et al. (2015,2014) [1,2]). Herein we provide the data regarding the effects of HLD6-associated tubulin beta 4A (TUBB4A) mutations on the properties