IkappaB kinase-alpha (IKK-alpha) exhibits protein-kinase-dependent and -independent functions. Its kinase activity is required for lymphoid organogenesis and mammary gland development, whereas a kinase-independent activity is required for epidermal keratinocyte differentiation. In addition to failed epidermal differentiation, IKK-alpha-deficient mice exhibit abnormal skeletal and craniofacial morphogenesis. As similar defects are not exhibited by mice that experience systemic inhibition of NF-kappaB, we postulated that the morphogenetic defects in IKK-alpha-deficient mice are not caused by reduced NF-kappaB activity but instead are due to failed epidermal differentiation that disrupts proper epidermal-mesodermal interactions. We tested this hypothesis by introducing an epidermal-specific Ikka (also known as Chuk) transgene into IKK-alpha-deficient mice. Mice lacking IKK-alpha in all cell types including bone and cartilage, but not in basal epidermal keratinocytes, exhibit normal epidermal differentiation and skeletal morphology. Thus, epidermal differentiation is required for proper morphogenesis of mesodermally derived skeletal elements. One way by which IKK-alpha controls skeletal and craniofacial morphogenesis is by repressing expression of fibroblast growth factor (FGF) family members, such as FGF8, whose expression is specifically elevated in the limb bud ectoderm of IKK-alpha-deficient mice.
Cell-cycle exit and differentiation of suprabasal epidermal keratinocytes require nuclear IB kinase ␣ (IKK␣), but not its protein kinase activity. IKK␣ also is a suppressor of squamous cell carcinoma (SCC), but its mode of action remains elusive. Postulating that IKK␣ may serve as a transcriptional regulator in keratinocytes, we searched for cell-cycle-related genes that could illuminate this function. IKK␣ was found to control several Myc antagonists, including Mad1, Mad2, and Ovol1, through the association with TGF-regulated Smad2/3 transcription factors and is required for Smad3 recruitment to at least one of these targets. Surprisingly, Smad2/3-dependent Mad1 induction and keratinocyte differentiation are independent of Smad4, the almost universal coregulator of canonical TGF signaling. IKK␣ also is needed for nuclear accumulation of activated Smad2/3 in the epidermis, and Smad2/3 are required for epidermal differentiation. We suggest that a TGF-Smad2/3-IKK␣ axis is a critical Smad4-independent regulator of keratinocyte proliferation and differentiation.epidermis ͉ cornification ͉ terminal differentiation A critical mediator of NF-B activation (1), IB kinase (IKK) consists of two catalytic subunits, IKK␣ and IKK (2-5), and a regulatory subunit, IKK␥/NEMO (6, 7). Despite structural similarity, IKK␣ and IKK have nonredundant functions, with IKK being the predominant IKK (1, 8) and IKK␣ being a critical regulator of keratinocyte differentiation (9, 10). Without IKK␣, epidermal keratinocytes exhibit enhanced proliferation and failure to differentiate. Consequently, Ikk␣ Ϫ/Ϫ mice are born enshrouded in a taut and thickened, nonstratified, epidermal sheet devoid of barrier function.The mammalian epidermis is a stratified squamous epithelium in which basal keratinocytes undergo asymmetric cell divisions, giving rise to nonproliferative progeny that embark on a differentiation program as they delaminate and move upward through the spinous and granular layers before generating the cornified layer, which provides the crucial barrier function (11, 12). Without IKK␣, this process is blocked, and basal keratinocytes fail to exit the cell cycle (9, 10, 13). Isolated Ikk␣ Ϫ/Ϫ keratinocytes proliferate uncontrollably and do not respond to differentiation-inducing signals such as high Ca 2ϩ (9, 13). The reexpression of IKK␣ in Ikk␣ Ϫ/Ϫ keratinocytes induces growth arrest and allows terminal differentiation, but this function depends neither on IKK␣'s protein kinase activity nor on NF-B. Instead, it requires nuclear accumulation of IKK␣ (14).Recently, IKK␣ was identified as a tumor suppressor in squamous cell carcinoma (SCC), a type of cancer derived from squamous epithelia of the skin, oral and nasal cavities, esophagus, and other sites (15). Decreased nuclear IKK␣ expression was found in about one third of oral SCCs, mainly those that exhibit poorly differentiated phenotype and poor prognosis (16). These results strongly suggest that loss of nuclear IKK␣ contributes to malignant conversion of keratinocytes to less dif...
Polyethylene materials are a serious environmental concern as their nondegradable nature allows them to persist in the environment. Recent studies have shown that polyethylene can be degraded by microbes at a very slow rate, whereby detectable changes are evident after several years. In the present study, we report the degradation of low-density polyethylene by Pseudomonas sp. AKS2. Unlike the previous reports, degradation by Pseudomonas sp. AKS2 is relatively fast as it can degrade 5 ± 1 % of the starting material in 45 days without prior oxidation. This degradation can be altered by agents that modulate hydrophobic interaction between polythene and the microbe. As mineral oil promotes hydrophobic interactions, it enhances bacterial attachment to the polymer surface. This enhanced attachment results in increased biofilm formation and enhanced polymer degradation. In contrast, Tween 80 reduces bacterial attachment to the polymer surface by lowering hydrophobic interactions and thereby reduces polymer degradation. Thus, this study establishes a correlation between hydrophobic interaction and polymer degradation and also relates the biofilm formation ability of bacteria to polymer degrading potential.
Aim: Polyethylene succinate (PES) contains hydrolysable ester bonds that make it a potential substitute for polyethylene (PE) and polypropylene (PP). Towards bioremediation of PES, we have already reported that a new strain of Pseudomonas, Pseudomonas sp. AKS2, can efficiently degrade PES and hypothesized that cell surface hydrophobicity plays an important role in this degradation process. In this study, our efforts were targeted towards establishing a correlation between cell surface hydrophobicity and PES degradation. Methods and Results: We have manipulated cell surface hydrophobicity of AKS2 by varying concentrations of glucose and ammonium sulphate in the growth medium and subsequently examined the extent of PES degradation. We observed an increase in PES degradation by AKS2 with an increase in cell surface hydrophobicity. The increased surface hydrophobicity caused an enhanced biofilm formation on PES surface that resulted in better polymer degradation. Conclusion:The current study establishes a direct correlation between cell surface hydrophobicity of an organism and its potential to degrade a nonpolar polymer like PES. Significance and Impact of the Study: Cell surface hydrophobicity manipulation can be used as an important strategy to increase bioremediation of nonpolar polymer like PES.
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