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Patterson, M. R.

Publications and source records attributed to Patterson, M. R..

2 recordsLinked to original sources

Time scales of mixing in an imperforate scleractinian coelenteron

Coelentera are the largest components by volume in the gastrovascular system connecting polyps in a scleractinian colony. Thus to understand colony connectivity which is predicted to affect corals response to environmental change, we must first describe the dynamics inside these gastric cavities of individual polyps. We determined key time scales of mixing in coelentera by using microelectrodes to measure oxygen concentration after a light-to-dark transition in three polyps each of three colonies of Montastraea cavernosa in the laboratory. The gastrovascular system was modeled as an electrical network where voltage represents oxygen concentration, current represents oxygen flux, capacitors represent volume compartments, and resistors represent impedance to oxygen flux. The time constant of mixing, defined as the time needed for the system to disperse 63.2% of the fluid in the coelenteron, was determined from the oxygen dynamics in the coelenteron as modeled by a resistor-capacitor network. Time constants were on the order of three minutes and oxygen dynamics were well fit by the model prediction. However, as polyps depleted oxygen, we observed small magnitude (~ 0.1 ppm), high-frequency fluctuations in oxygen concentration. A power spectral density analysis identified two time scales of high-frequency mixing in the coelenteron. The greatest variance occurred at a period of 48.3 {+/-} 2.8 seconds, with a secondary peak seen at 35.9 {+/-} 2.3 seconds. The microenvironment within polyps of M. cavernosa can respond as fast or faster than their external environment can fluctuate, thus scleractinian polyps have the capacity to mediate their response to changing environmental conditions.

physiology

The deubiquitinase (DUB) USP13 promotes Mcl-1 stabilisation in cervical cancer

Ubiquitination is a critical regulator of cellular homeostasis. Aberrations in the addition or removal of ubiquitin can result in the development of cancer and key components of the ubiquitination machinery serve as oncogenes or tumour suppressors. An emerging target in the development of cancer therapeutics are the deubiquitinase (DUB) enzymes that remove ubiquitin from protein substrates. Whether this class of enzyme plays a role in cervical cancer has not been fully explored. By interrogating the cervical cancer data from the TCGA consortium, we noted that the DUB USP13 is amplified in approximately 15% of cervical cancer cases. We confirmed that USP13 expression was increased in cervical cancer cell lines, cytology samples from patients with cervical disease and in cervical cancer tissue. Depletion of USP13 inhibited cervical cancer cell proliferation. Mechanistically, USP13 bound to, deubiquitinated and stabilised Mcl-1, a pivotal member of the anti-apoptotic Bcl-2 family and the reduced Mcl-1 expression contributed to the observed proliferative defect. Importantly, the expression of USP13 and Mcl-1 proteins correlated in cervical cancer tissue. Finally, we demonstrated that depletion of USP13 expression or inhibition of USP13 enzymatic activity increased the sensitivity of cervical cancer cells to the BH3 mimetic inhibitor ABT-263. Together, our data demonstrates that USP13 is a potential oncogene in cervical cancer that functions to stabilise the pro-survival protein Mcl-1, offering a potential therapeutic target for these cancers.

microbiology