A cat cloned by nuclear transplantation

Sheep, mice, cattle, goats and pigs have all been cloned by transfer of a donor cell nucleus into an enucleated ovum, and now we add the successful cloning of a cat (Felis domesticus) to this list. However, this cloning technology may not be readily extendable to other mammalian species if our understanding of their reproductive processes is limited or if there are species-specific obstacles.     

一个美国人类学家的中国情结

人类学在聚焦世界各地人们的生活及其方式的过程中,一直致力于成为一门客观性的科学。最近,女性人类学者们的一些活动则为表达主观观点,传达个人情感及检验人类学者和研究群体间的关系开辟了道路。这篇文章审视了我个人一生对中国的美好情感,而我的这种情感于 2000 年参加在北京举行的IUAES(国际人类学民族学联合会中期会议)时达到高潮。     

Microbial starch-binding domains are superior to granule-bound starch synthase I for anchoring luciferase to potato starch granules

Microbial starch-binding domains (SBD) and granule-bound starch synthase I (GBSSI) are proteins which are accumulated in potato starch granules. The efficiency of SBD and GBSSI for targeting active luciferase reporter proteins to granules during starch biosynthesis was compared. GBSSI or SBD sequences were fused to the N- or C-terminus of the luciferase (LUC) gene, via an artificial Pro-Thr encoding linker sequence. The genes were introduced into an amylose-free (amf) potato mutant. It appeared that SBD was superior to GBSSI as a targeting sequence, mainly because the luciferase retained higher activity in the SBD-containing fusion proteins than in the GBSSI-containing ones.     

Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J mice.

Pigmentary glaucoma is a significant cause of human blindness. Abnormally liberated iris pigment and cell debris enter the ocular drainage structures, leading to increased intraocular pressure (IOP) and glaucoma. DBA/2J (D2) mice develop a form of pigmentary glaucoma involving iris pigment dispersion (IPD) and iris stromal atrophy (ISA). Using high-resolution mapping techniques, sequencing and functional genetic tests, we show that IPD and ISA result from mutations in related genes encoding melanosomal proteins. IPD is caused by a premature stop codon mutation in the Gpnmb (GpnmbR150X) gene, as proved by the occurrence of IPD only in D2 mice that are homozygous with respect to GpnmbR150X; otherwise, similar D2 mice that are not homozygous for GpnmbR150X do not develop IPD. ISA is caused by the recessive Tyrp1b mutant allele and rescued by the transgenic introduction of wildtype Tyrp1. We hypothesize that IPD and ISA alter melanosomes, allowing toxic intermediates of pigment production to leak from melanosomes, causing iris disease and subsequent pigmentary glaucoma. This is supported by the rescue of IPD and ISA in D2 eyes with substantially decreased pigment production. These data indicate that pigment production and mutant melanosomal protein genes may contribute to human pigmentary glaucoma. The fact that hypopigmentation profoundly alleviates the D2 disease indicates that therapeutic strategies designed to decrease pigment production may be beneficial in human pigmentary glaucoma.