近日，國家著名雜志Applied Microbiology and Biotechnology刊登了中科院亞熱帶農(nóng)業(yè)生態(tài)研究所研究人員的研究成果“Long-term field fertilization alters the diversity of autotrophic bacteria based on the ribulose-1,5-biphosphate carboxylase/oxygenase (RubisCO) large-subunit genes in paddy soil,。”,，文章中，研究人員揭示了長(zhǎng)期施肥對(duì)土壤固碳細(xì)菌群落結(jié)構(gòu),、多樣性及數(shù)量均有顯著的影響,。
生物固碳是陸地生態(tài)系統(tǒng)中最直接有效的二氧化碳固定途徑，其中具有固碳功能的微生物分布廣泛,，它們有很強(qiáng)的環(huán)境適應(yīng)能力,。從整個(gè)生物圈的物質(zhì)、能量流來看,，二氧化碳的微生物固定是一支絕不容忽視的生物固碳力量,。因此,，研究微生物固定二氧化碳的生態(tài)環(huán)境效應(yīng)具現(xiàn)實(shí)意義。
cbbL基因編碼的核酮糖-1, 5-二磷酸梭化酶/加氧酶（RubisCO）是卡爾文循環(huán)中的關(guān)鍵酶,，該酶催化卡爾文循環(huán)中的第一步CO2固定反應(yīng),。然而，目前關(guān)于固碳自養(yǎng)菌cbbL基因的分子生態(tài)學(xué)研究主要集中在旱作系統(tǒng),，對(duì)于稻田土壤,，特別是長(zhǎng)期不同施肥制度對(duì)稻田土壤固碳自養(yǎng)菌群落及多樣性影響的研究未見報(bào)道,。
中科院亞熱帶農(nóng)業(yè)生態(tài)研究所研究員吳金水研究組以湖南寧鄉(xiāng),、桃江、望城國家級(jí)稻田肥力變化長(zhǎng)期定位試驗(yàn)為平臺(tái),，采用PCR-克隆測(cè)序和實(shí)時(shí)熒光定量（Real-time）PCR技術(shù),，研究不施肥（CK）,，氮磷鉀肥（NPK）和秸稈還田（NPKS）3種長(zhǎng)期施肥制度對(duì)稻田土壤固碳自養(yǎng)菌群落結(jié)構(gòu)及數(shù)量的影響,。
通過分析固碳細(xì)菌cbbL基因文庫發(fā)現(xiàn)，三個(gè)地點(diǎn)的cbbL含有的細(xì)菌群落以兼性自養(yǎng)菌為主,，如沼澤紅假單胞菌,，Bradyrhizobium japonicum和氧產(chǎn)堿桿菌。長(zhǎng)期施肥導(dǎo)致土壤固碳自養(yǎng)菌種群結(jié)構(gòu)產(chǎn)生了明顯差異,，NPK和NPKS處理中兼性自養(yǎng)固碳菌群落優(yōu)勢(shì)增加,，而嚴(yán)格自養(yǎng)固碳菌生長(zhǎng)受到抑制,。細(xì)菌cbbL基因拷貝數(shù)（3–8×108 copies g soil-1）與稻田土壤固碳關(guān)鍵酶Rubisco活性（0.40–1.76 nmol CO2 g soil-1min-1）活性呈顯著相關(guān)性,，并且隨著施肥量的增加而增大。ACC分析表明,，土壤有機(jī)碳含量和pH是細(xì)菌cbbL群落組成、豐度,、多樣性等最重要的影響因子,。
上述結(jié)果表明長(zhǎng)期施肥對(duì)土壤固碳細(xì)菌群落結(jié)構(gòu)、多樣性及數(shù)量均有顯著的影響,。本研究結(jié)果可為深入探討稻田土壤微生物固碳潛力及其影響機(jī)理提供有力的依據(jù),。該研究組的博士研究生袁紅朝是該論文的第一作者,。該研究得到了中國科學(xué)院,、國家外國專家局創(chuàng)新團(tuán)隊(duì)國際合作伙伴計(jì)劃、國家自然科學(xué)基金委和中科院知識(shí)創(chuàng)新工程青年人才領(lǐng)域前沿項(xiàng)目的資助,。(生物谷Bioon.com)
doi:10.1007/s00253-011-3760-y
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Long-term field fertilization alters the diversity of autotrophic bacteria based on the ribulose-1,5-biphosphate carboxylase/oxygenase (RubisCO) large-subunit genes in paddy soil,。
Hongzhao Yuan, Tida Ge, Xiaohong Wu, Shoulong Liu, Chengli Tong, Hongling Qin, Minna Wu, Wenxue Wei and Jinshui Wu
Many mutations, including those that cause disease, only have a detrimental effect in a subset of individuals. The reasons for this are usually unknown, but may include additional genetic variation and environmental risk factors1. However, phenotypic discordance remains even in the absence of genetic variation, for example between monozygotic twins2, and incomplete penetrance of mutations is frequent in isogenic model organisms in homogeneous environments3, 4. Here we propose a model for incomplete penetrance based on genetic interaction networks5, 6. Using Caenorhabditis elegans as a model system, we identify two compensation mechanisms that vary among individuals and influence mutation outcome. First, feedback induction of an ancestral gene duplicate differs across individuals, with high expression masking the effects of a mutation. This supports the hypothesis that redundancy is maintained in genomes to buffer stochastic developmental failure7. Second, during normal embryonic development we find that there is substantial variation in the induction of molecular chaperones such as Hsp90 (DAF-21). Chaperones act as promiscuous buffers of genetic variation8, 9, and embryos with stronger induction of Hsp90 are less likely to be affected by an inherited mutation. Simultaneously quantifying the variation in these two independent responses allows the phenotypic outcome of a mutation to be more accurately predicted in individuals. Our model and methodology provide a framework for dissecting the causes of incomplete penetrance. Further, the results establish that inter-individual variation in both specific and more general buffering systems combine to determine the outcome inherited mutations in each individual.
