Regulation of enzymes involved in the sulphur-assimilatory pathway

The regulation of enzymes involved in sulphate assimilation in plants has been investigated. Extractable activity of ATP sulphurylase (the first enzyme of the assimilatory pathway) has been shown to be regulated by sulphate availability and O-acctylserine (OAS) supply. OAS addition to the medium increased extractable activity and was able, at least partially, to overcome the repression of extraclable activity observed by supply of sulphate and cysteine. Cysteine synthase, the final enzyme of the cysteine biosynthetic pathway, was not regulated under these conditions.     

A cytokinin perception mutant colonized by Rhizobium in the absence of nodule organogenesis

In legumes, Nod-factor signaling by rhizobia initiates the development of the nitrogen-fixing nodule symbiosis, but the direct cell division stimulus that brings about nodule primordia inception in the root cortex remains obscure. We showed that Lotus japonicus plants homozygous for a mutation in the HYPERINFECTED 1 (HIT1) locus exhibit abundant infection-thread formation but fail to initiate timely cortical cell divisions in response to rhizobial signaling. We demonstrated that the corresponding gene encodes a cytokinin receptor that is required for the activation of the nodule inception regulator Nin and nodule organogenesis.     

Molecular phylogenetics of mastodon and Tyrannosaurus rex

We report a molecular phylogeny for a nonavian dinosaur, extending our knowledge of trait evolution within nonavian dinosaurs into the macromolecular level of biological organization. Fragments of collagen alpha1(I) and alpha2(I) proteins extracted from fossil bones of Tyrannosaurus rex and Mammut americanum (mastodon) were analyzed with a variety of phylogenetic methods. Despite missing sequence data, the mastodon groups with elephant and the T. rex groups with birds, consistent with predictions based on genetic and morphological data for mastodon and on morphological data for T. rex. Our findings suggest that molecular data from long-extinct organisms may have the potential for resolving relationships at critical areas in the vertebrate evolutionary tree that have, so far, been phylogenetically intractable.     

土壤拮抗链霉菌R15菌株发酵产物的抑菌作用

对一株土壤拮抗链霉菌(Streptomycespp.)R15菌株发酵液的抑菌效果、热稳定性和酸碱稳定性以及作用机制进行了初步研究。结果表明,拮抗链霉菌R15发酵液对棉花枯萎病菌分生孢子萌发抑制作用强,抑制率达98.37%。烟草赤星病菌孢子萌发后芽管顶端膨大成球形,芽管停止生长;烟草炭疽病菌孢子萌发后不能产生附着胞,且芽管顶端有突起。处理烟草黑胫病菌和辣椒疫霉病菌菌丝畸变、扭曲、菌丝壁消解;R15通过菌丝缠绕、穿透、紧贴的方式重寄生于烟草黑胫病菌菌丝上,致使菌丝断裂。链霉菌R15发酵液的热稳定性和酸碱稳定性较强,在20～55℃,pH3～9范围内都具有抑菌活性。     

Inactivation of TNF signaling by rationally designed dominant-negative TNF variants

Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.     

Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia

Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations but also the cellular framework in which they arise and function. Here we explore the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is characterized by a chromosomal translocation generating a TEL-AML1 fusion gene. We identify a cell compartment in leukemic children that can propagate leukemia when transplanted in mice. By studying a monochorionic twin pair, one preleukemic and one with frank leukemia, we establish the lineal relationship between these "cancer-propagating" cells and the preleukemic cell in which the TEL-AML1 fusion first arises or has functional impact. Analysis of TEL-AML1-transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties.