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Ivy Amor F. Lambio,Marnelli S. Alviola,Cristian C. Lucañas,Aimee Lynn A. Barrion-Dupo,Camille Faith D. Duran,Ma. Francia Kyla M. Cammayo,Kirk J. Taray,Orlando L. Eusebio,Ireneo L. Lit Jr. 국립중앙과학관 2024 Journal of Asia-Pacific Biodiversity Vol.17 No.1
A new record of a holoparasitic plant is hereby reported to thrive in the twilight zone of Dry Cave I,Tayabas, Quezon Province, Philippines. This is the first record of a Balanophora species thriving withincave ecosystems. Based on the observed production of white sap from the roots inside the cave and apreliminary survey of trees above the cave, the probable host of the Balanophora abbreviata is Ficus sp. (Moraceae). Fig trees are capable of producing deeply penetrating and lithophytic roots. Based on theexistence of various arthropods in and within the vicinity of the plant clumps, the possible role ofB. abbreviata as part of the food web within Dry Cave I is also discussed.
Garbes, L.,Kim, K.,Riesz, A.,Hoyer-Kuhn, H.,Beleggia, F.,Bevot, A.,Kim, M.,Huh, Y.,Kweon, H.S.,Savarirayan, R.,Amor, D.,Kakadia, Purvi M.,Lindig, T.,Kagan, K.,Becker, J.,Boyadjiev, Simeon A.,Wollnik, University of Chicago Press [etc.] 2015 American journal of human genetics Vol.96 No.3
As a result of a whole-exome sequencing study, we report three mutant alleles in SEC24D, a gene encoding a component of the COPII complex involved in protein export from the ER: the truncating mutation c.613C>T (p.Gln205<SUP>*</SUP>) and the missense mutations c.3044C>T (p.Ser1015Phe, located in a cargo-binding pocket) and c.2933A>C (p.Gln978Pro, located in the gelsolin-like domain). Three individuals from two families affected by a similar skeletal phenotype were each compound heterozygous for two of these mutant alleles, with c.3044C>T being embedded in a 14 Mb founder haplotype shared by all three. The affected individuals were a 7-year-old boy with a phenotype most closely resembling Cole-Carpenter syndrome and two fetuses initially suspected to have a severe type of osteogenesis imperfecta. All three displayed a severely disturbed ossification of the skull and multiple fractures with prenatal onset. The 7-year-old boy had short stature and craniofacial malformations including macrocephaly, midface hypoplasia, micrognathia, frontal bossing, and down-slanting palpebral fissures. Electron and immunofluorescence microscopy of skin fibroblasts of this individual revealed that ER export of procollagen was inefficient and that ER tubules were dilated, faithfully reproducing the cellular phenotype of individuals with cranio-lentico-sutural dysplasia (CLSD). CLSD is caused by SEC23A mutations and displays a largely overlapping craniofacial phenotype, but it is not characterized by generalized bone fragility and presented with cataracts in the original family described. The cellular and morphological phenotypes we report are in concordance with the phenotypes described for the Sec24d-deficient fish mutants vbi (medaka) and bulldog (zebrafish).