Yifei Zhu
Trans. Amer. Math. Soc. 373 (2020), 3733-3764.
Abstract, references and article information

Yu. V. Kozachenko and I. V. Rozora
Theor. Probability and Math. Statist. 99 (2020), 113-124.
Abstract, references and article information

T. Bodnar, S. Mazur, S. Muhinyuza and N. Parolya
Theor. Probability and Math. Statist. 99 (2020), 39-52.
Abstract, references and article information

How to optimise your website, increase conversions and monetise your online offering

Secretary for Justice Teresa Cheng today refuted suggestions that the law prohibiting group gatherings to combat the COVID-19 epidemic was being misused to crack down on protests and people's freedoms.

During a media session, Ms Cheng responded to criticisms from some legislators that Police were abusing the measure to clamp down on protests.

She said: “The Government respects and protects the freedoms that are set out in our laws, Basic Law and the Hong Kong Bill of Rights Ordinance. However, these freedoms are not absolute. Insofar as they violate the laws, then of course appropriate actions will have to be taken.”

The Government had earlier introduced the Prevention & Control of Disease (Prohibition on Group Gathering) Regulation (Cap. 599G) to prohibit group gatherings with more than four people in public places with a view to combating COVID-19.

The regulation was made in accordance with the Prevention & Control of Disease Ordinance (Cap. 599).

“Cap. 599G is enforced under Cap. 599 as a matter of the public health emergency situation that is facing Hong Kong at the moment. It is promulgated to encourage social distancing. It is not with any other motive except for the safety and health of the people in Hong Kong.

“I hope that you will all comply with it in spirit and in form, so that you will not gather and thereby extend Hong Kong's position in this public health emergency situation. That is the only way by which we can get back to normal life as soon as possible.”

In response to a reporter's question on the relevant provisions in the Basic Law that pertain to the Liaison Office of the Central People's Government in the Hong Kong Special Administrative Region, Ms Cheng remarked that the liaison office must also comply with Hong Kong laws.

“The Central People's Government as defined in the Constitution Law is actually the State Council, and therefore when one looks at the whole thing about the Constitution Law, Article 5 of the Constitution Law states unequivocally that every body that is set up will have to comply with the relevant laws and the Constitution Law.

“In other words, the liaison office will have to obey and comply with the laws in Hong Kong.”

The Government issued directions in the Gazette today to close bars and premises selling liquor for 14 days from 6pm on April 3.

The Secretary for Food & Health issued the directions in accordance with the Prevention & Control of Disease (Requirements & Directions) (Business & Premises) Regulation.

The directions include the closure of bars and pubs, as well as any part of a catering business premise or a clubhouse mainly used for the sale or supply of intoxicating liquors for consumption.

The new measures were introduced due to the emergence of 62 confirmed COVID-19 cases related to the bar and band cluster with further spread to an additional 14 cases who had not visited bars.

The Government on April 1 introduced directions on the closure of karaoke, mahjong-tin kau and nightclub establishments as well as the suspension of karaoke and mahjong-tin kau activities in catering premises and clubhouses.

It has also been reviewing the feasibility of relevant measures and will make timely adjustments according to the latest developments of the disease.

The onset of COVID-19 has severely affected our economy and the legal sector was not spared. I have discussed with some of the representatives from the industry and we have carefully considered their suggestions with relevant government departments.

On Wednesday, the Government announced another package of measures to support individuals and businesses affected by COVID-19. Two of the measures are relevant to the legal sector: the establishment of LawTech Fund and the COVID-19 Online Dispute Resolution (ODR) Scheme. Today, I would like to share with you the arrangement of the LawTech Fund.

The Government always attaches great importance to LawTech. In her 2018 Policy Address, the Chief Executive supported the development of an online platform by non-government organisations to facilitate the provision of efficient and cost-effective online dispute resolution services in Hong Kong. The Government would allocate funding for the development of this project.

At the Ceremonial Opening of the Legal Year 2019, I emphasised the importance of making use of technology in providing legal services, citing the United Nations General Assembly in 2016 in observing that online dispute resolution "can assist the parties in resolving the dispute in a simple, fast, flexible, and secure manner, without the need for physical presence at a meeting or hearing". The Asia-Pacific Economic Cooperation had responded to the call and embarked on a project to establish an ODR framework with micro, small and medium-sized enterprises as major beneficiaries.

Almost 18% of the annual caseload of the courts at all levels have been affected in the first two months of the General Adjourned Period since January 29. The Judiciary has earlier started using video-conferencing facilities for remote hearings on suitable civil cases at the High Court. The media reported the first hearing conducted through video-conferencing, quoting the legal representatives of both parties being supportive of the Judiciary's new measures in view of the low cost and smooth operation.

Given the severe impact brought by COVID-19, the Judiciary has been exploring the use of various technological means in conducting different types of hearings to address the growing backlog of cases caused by the postponement of hearings. The legal sector should also take this opportunity to review the wider use of LawTech and enhance their technological capability. The Government introduced the LawTech Fund, which aims to assist some small and medium size law firms/barristers' chambers in procuring and upgrading information technology systems (such as video-conferencing facilities) and attending LawTech training courses. This will be conducive to the promotion of use of technologies in the provision of legal services.

Under the scheme, law firms and chambers with not more than five practicing lawyers are eligible for application. Each firm/chamber will be eligible for a reimbursable amount of up to $50,000. Application for the fund will be jointly administered by the Law Society of Hong Kong and the Hong Kong Bar Association. The details will be announced soon and the fund will be opened for application next month.

Other measures announced by the Government include: Enhancement of SME Financing Guarantee Scheme, Employment Support Scheme under which the Government will provide wage subsidy to eligible employers to retain employees (details will be available soon), as well as the creation of some time-limited jobs by the Department of Justice.

Government measures alone, however, would not be adequate. We must all stand united in solidarity to fight the virus and support Hong Kong.

Secretary for Justice Teresa Cheng wrote this article and posted it on her blog on April 11.

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Banks and financial institutions taking part in providing mortgage loans for the Housing Authority Subsidised Sale Flats Scheme (SSFS) may offer a mortgage principal moratorium plan to the scheme’s mortgagors.

The authority today wrote to these institutions to confirm and agree that such a plan is applicable for SSFS flats.

Principal repayment may be deferred for a maximum 12-month period and the mortgage loan repayment period may be extended correspondingly by a maximum of 12 months.

The principal moratorium period may commence by December 31 this year at the latest.

The arrangement is applicable to the Home Ownership Scheme, the Private Sector Participation Scheme, the Buy or Rent Option Scheme, the Tenants Purchase Scheme and the Green Form Subsidised Home Ownership Scheme in the primary market and under the Secondary Market Scheme.

To encourage participating financial institutions to provide mortgage loans and better mortgage terms for SSFS flat purchasers, the authority provides a mortgage default guarantee for them.

It undertakes to meet the shortfall in repayment in the event of default by the borrowers under specified circumstances during the guarantee period.

Due to the requirements in the guarantee deed on the mortgage loan period and the monthly instalment amount, participating financial institutions may not be able to offer a mortgage principal moratorium plan to SSFS flat owners.

In light of the economic downturn arising from the COVID-19 outbreak, the authority confirmed today that a mortgage principal moratorium plan is applicable for SSFS flats.

The move will encourage participating financial institutions to offer such a plan to SSFS flat owners, reducing their burden of mortgage repayment.

Ekta Singh
Nov 1, 2012; 25:217-221
From Research to Practice

The Mortgage Corporation today announced that the pilot scheme for fixed-rate mortgages will start receiving applications from May 7.

The aggregate loan amount of the Fixed-rate Mortgage Pilot Scheme is $1 billion, subject to a maximum loan amount of each private residential mortgage of $10 million.

Financial Secretary Paul Chan said the pilot scheme, announced in the 2020-21 Budget, provides an alternative financing option to homebuyers for mitigating their risks arising from interest rate volatility, thereby promoting the development of the mortgage market in the long run.

In response to the change in market interest rates, mortgage interest rates under the pilot scheme have been lowered, as compared to the levels previously announced in the Budget. The interest rates per annum for 10, 15 and 20 years are 2.55%, 2.65% and 2.75%.

Mortgages under the pilot scheme will be offered through Bank of China, Chong Hing Bank, Dah Sing Bank, Industrial & Commercial Bank of China, Shanghai Commercial Bank, Standard Chartered Bank and The Bank of East Asia.

At the end of the fixed-rate period, borrowers may either re-fix the mortgage rate under fixed-rate mortgages or convert the mortgage to a loan on a floating rate, which is the prime rate minus 2.35%.

The pilot scheme will be effective until October 31.

(University of South Florida (USF Health)) A new preclinical study by researchers at the University of South Florida Health (USF Health) Morsani College of Medicine and Johns Hopkins University School of Medicine offers promise of a specific treatment for NEC, a rare inflammatory bowel disease that is a leading cause of death in premature infants. The team found that inhibiting the inflammatory and blood-clotting molecule thrombin with targeted nanotherapy can protect against NEC-like injury in newborn mice.

(To watch the full press briefing with sign language interpretation, click here.)

A recovered COVID-19 patient has tested positive for the virus again, the Hospital Authority announced today.

The authority’s Chief Manager (Quality & Standards) Dr Lau Ka-hin told a media briefing this afternoon that the patient was first admitted to Queen Mary Hospital on March 24 after having fever for a week. He subsequently tested positive for COVID-19.

He was discharged on April 16 after two consecutive negative tests for the virus.

Dr Lau said: "The patient presented to the Accident & Emergency Department of Queen Mary Hospital on May 5 because of some abdominal pain and diarrhoea.

"He was admitted to our hospital and was found to have a positive result for COVID-19 in the throat saliva, but the cycle threshold value is very high - nearly 36.

"The experts consider that this is the residual virus left in the patient’s body, which is not infective, and it is not likely to be a reinfection at this moment."

He added that the patient is in a stable condition.

Hypersecretion of glucagon from pancreatic α-cells strongly contributes to diabetic hyperglycemia. Moreover, failure of α-cells to increase glucagon secretion in response to falling blood glucose concentrations compromises the defense against hypoglycemia, a common complication in diabetes therapy. However, the mechanisms underlying glucose regulation of glucagon secretion are poorly understood and likely involve both α-cell–intrinsic and intraislet paracrine signaling. Among paracrine factors, glucose-stimulated release of the GABA metabolite γ-hydroxybutyric acid (GHB) from pancreatic β-cells might mediate glucose suppression of glucagon release via GHB receptors on α-cells. However, the direct effects of GHB on α-cell signaling and glucagon release have not been investigated. Here, we found that GHB (4–10 μm) lacked effects on the cytoplasmic concentrations of the secretion-regulating messengers Ca2+ and cAMP in mouse α-cells. Glucagon secretion from perifused mouse islets was also unaffected by GHB at both 1 and 7 mm glucose. The GHB receptor agonist 3-chloropropanoic acid and the antagonist NCS-382 had no effects on glucagon secretion and did not affect stimulation of secretion induced by a drop in glucose from 7 to 1 mm. Inhibition of endogenous GHB formation with the GABA transaminase inhibitor vigabatrin also failed to influence glucagon secretion at 1 mm glucose and did not prevent the suppressive effect of 7 mm glucose. In human islets, GHB tended to stimulate glucagon secretion at 1 mm glucose, an effect mimicked by 3-chloropropanoic acid. We conclude that GHB does not mediate the inhibitory effect of glucose on glucagon secretion.

The canonical pathway of eicosanoid production in most mammalian cells is initiated by phospholipase A2-mediated release of arachidonic acid, followed by its enzymatic oxidation resulting in a vast array of eicosanoid products. However, recent work has demonstrated that the major phospholipase in mitochondria, iPLA2γ (patatin-like phospholipase domain containing 8 (PNPLA8)), possesses sn-1 specificity, with polyunsaturated fatty acids at the sn-2 position generating polyunsaturated sn-2-acyl lysophospholipids. Through strategic chemical derivatization, chiral chromatographic separation, and multistage tandem MS, here we first demonstrate that human platelet-type 12-lipoxygenase (12-LOX) can directly catalyze the regioselective and stereospecific oxidation of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-AA-LPE). Next, we identified these two eicosanoid-lysophospholipids in murine myocardium and in isolated platelets. Moreover, we observed robust increases in 2-AA-LPC, 2-AA-LPE, and their downstream 12-LOX oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LPE, in calcium ionophore (A23187)-stimulated murine platelets. Mechanistically, genetic ablation of iPLA2γ markedly decreased the calcium-stimulated production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse platelets. Importantly, a potent and selective 12-LOX inhibitor, ML355, significantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets. Furthermore, we found that aging is accompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenuated by iPLA2γ genetic ablation. Collectively, these results identify previously unknown iPLA2γ-initiated signaling pathways mediated by direct 12-LOX oxidation of 2-AA-LPC and 2-AA-LPE. This oxidation generates previously unrecognized eicosanoid-lysophospholipids that may serve as biomarkers for age-related diseases and could potentially be used as targets in therapeutic interventions.

β-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide. Previously, we demonstrated that lysosomal GBA1 and nonlysosomal GBA2 possess not only GlcCer hydrolase activity, but also transglucosylation activity to transfer the glucose residue from GlcCer to cholesterol to form β-cholesterylglucoside (β-GlcChol) in vitro. β-GlcChol is a member of sterylglycosides present in diverse species. How GBA1 and GBA2 mediate β-GlcChol metabolism in the brain is unknown. Here, we purified and characterized sterylglycosides from rodent and fish brains. Although glucose is thought to be the sole carbohydrate component of sterylglycosides in vertebrates, structural analysis of rat brain sterylglycosides revealed the presence of galactosylated cholesterol (β-GalChol), in addition to β-GlcChol. Analyses of brain tissues from GBA2-deficient mice and GBA1- and/or GBA2-deficient Japanese rice fish (Oryzias latipes) revealed that GBA1 and GBA2 are responsible for β-GlcChol degradation and formation, respectively, and that both GBA1 and GBA2 are responsible for β-GalChol formation. Liquid chromatography–tandem MS revealed that β-GlcChol and β-GalChol are present throughout development from embryo to adult in the mouse brain. We found that β-GalChol expression depends on galactosylceramide (GalCer), and developmental onset of β-GalChol biosynthesis appeared to be during myelination. We also found that β-GlcChol and β-GalChol are secreted from neurons and glial cells in association with exosomes. In vitro enzyme assays confirmed that GBA1 and GBA2 have transgalactosylation activity to transfer the galactose residue from GalCer to cholesterol to form β-GalChol. This is the first report of the existence of β-GalChol in vertebrates and how β-GlcChol and β-GalChol are formed in the brain.

VOLUME 295 (2020) PAGES 3285–3300An incorrect graph was used in Fig. 5C. This error has now been corrected. Additionally, some of the statistics reported in the legend and text referring to Fig. 5C were incorrect. The F statistics for Fig. 5C should state Fken(3,16) = 7.454, p < 0.01; FCCCP(1,16) = 102.9, p < 0.0001; Finteraction(3,16) = 7.480, p < 0.01. This correction does not affect the results or conclusions of this work.jbc;295/17/5835/F5F1F5Figure 5C.

Cell-surface signaling (CSS) in Gram-negative bacteria involves highly conserved regulatory pathways that optimize gene expression by transducing extracellular environmental signals to the cytoplasm via inner-membrane sigma regulators. The molecular details of ferric siderophore-mediated activation of the iron import machinery through a sigma regulator are unclear. Here, we present the 1.56 Å resolution structure of the periplasmic complex of the C-terminal CSS domain (CCSSD) of PupR, the sigma regulator in the Pseudomonas capeferrum pseudobactin BN7/8 transport system, and the N-terminal signaling domain (NTSD) of PupB, an outer-membrane TonB-dependent transducer. The structure revealed that the CCSSD consists of two subdomains: a juxta-membrane subdomain, which has a novel all-β-fold, followed by a secretin/TonB, short N-terminal subdomain at the C terminus of the CCSSD, a previously unobserved topological arrangement of this domain. Using affinity pulldown assays, isothermal titration calorimetry, and thermal denaturation CD spectroscopy, we show that both subdomains are required for binding the NTSD with micromolar affinity and that NTSD binding improves CCSSD stability. Our findings prompt us to present a revised model of CSS wherein the CCSSD:NTSD complex forms prior to ferric-siderophore binding. Upon siderophore binding, conformational changes in the CCSSD enable regulated intramembrane proteolysis of the sigma regulator, ultimately resulting in transcriptional regulation.

Treatment of patients with chronic lymphocytic leukemia (CLL) with inhibitors of Bruton's tyrosine kinase (BTK), such as ibrutinib, is limited by primary or secondary resistance to this drug. Examinations of CLL patients with late relapses while on ibrutinib, which inhibits BTK's catalytic activity, revealed several mutations in BTK, most frequently resulting in the C481S substitution, and disclosed many mutations in PLCG2, encoding phospholipase C-γ2 (PLCγ2). The PLCγ2 variants typically do not exhibit constitutive activity in cell-free systems, leading to the suggestion that in intact cells they are hypersensitive to Rac family small GTPases or to the upstream kinases spleen-associated tyrosine kinase (SYK) and Lck/Yes-related novel tyrosine kinase (LYN). The sensitivity of the PLCγ2 variants to BTK itself has remained unknown. Here, using genetically-modified DT40 B lymphocytes, along with various biochemical assays, including analysis of PLCγ2-mediated inositol phosphate formation, inositol phospholipid assessments, fluorescence recovery after photobleaching (FRAP) static laser microscopy, and determination of intracellular calcium ([Ca2+]i), we show that various CLL-specific PLCγ2 variants such as PLCγ2S707Y are hyper-responsive to activated BTK, even in the absence of BTK's catalytic activity and independently of enhanced PLCγ2 phospholipid substrate supply. At high levels of B-cell receptor (BCR) activation, which may occur in individual CLL patients, catalytically-inactive BTK restored the ability of the BCR to mediate increases in [Ca2+]i. Because catalytically-inactive BTK is insensitive to active-site BTK inhibitors, the mechanism involving the noncatalytic BTK uncovered here may contribute to preexisting reduced sensitivity or even primary resistance of CLL to these drugs.

The dextransucrase DSR-OK from the Gram-positive bacterium Oenococcus kitaharae DSM17330 produces a dextran of the highest molar mass reported to date (∼109 g/mol). In this study, we selected a recombinant form, DSR-OKΔ1, to identify molecular determinants involved in the sugar polymerization mechanism and that confer its ability to produce a very-high-molar-mass polymer. In domain V of DSR-OK, we identified seven putative sugar-binding pockets characteristic of glycoside hydrolase 70 (GH70) glucansucrases that are known to be involved in glucan binding. We investigated their role in polymer synthesis through several approaches, including monitoring of dextran synthesis, affinity assays, sugar binding pocket deletions, site-directed mutagenesis, and construction of chimeric enzymes. Substitution of only two stacking aromatic residues in two consecutive sugar-binding pockets (variant DSR-OKΔ1-Y1162A-F1228A) induced quasi-complete loss of very-high-molar-mass dextran synthesis, resulting in production of only 10–13 kg/mol polymers. Moreover, the double mutation completely switched the semiprocessive mode of DSR-OKΔ1 toward a distributive one, highlighting the strong influence of these pockets on enzyme processivity. Finally, the position of each pocket relative to the active site also appeared to be important for polymer elongation. We propose that sugar-binding pockets spatially closer to the catalytic domain play a major role in the control of processivity. A deep structural characterization, if possible with large-molar-mass sugar ligands, would allow confirming this hypothesis.

Accumulating evidence suggests that brown adipose tissue (BAT) is a potential therapeutic target for managing obesity and related diseases. PGAM family member 5, mitochondrial serine/threonine protein phosphatase (PGAM5), is a protein phosphatase that resides in the mitochondria and regulates many biological processes, including cell death, mitophagy, and immune responses. Because BAT is a mitochondria-rich tissue, we have hypothesized that PGAM5 has a physiological function in BAT. We previously reported that PGAM5-knockout (KO) mice are resistant to severe metabolic stress. Importantly, lipid accumulation is suppressed in PGAM5-KO BAT, even under unstressed conditions, raising the possibility that PGAM5 deficiency stimulates lipid consumption. However, the mechanism underlying this observation is undetermined. Here, using an array of biochemical approaches, including quantitative RT-PCR, immunoblotting, and oxygen consumption assays, we show that PGAM5 negatively regulates energy expenditure in brown adipocytes. We found that PGAM5-KO brown adipocytes have an enhanced oxygen consumption rate and increased expression of uncoupling protein 1 (UCP1), a protein that increases energy consumption in the mitochondria. Mechanistically, we found that PGAM5 phosphatase activity and intramembrane cleavage are required for suppression of UCP1 activity. Furthermore, utilizing a genome-wide siRNA screen in HeLa cells to search for regulators of PGAM5 cleavage, we identified a set of candidate genes, including phosphatidylserine decarboxylase (PISD), which catalyzes the formation of phosphatidylethanolamine at the mitochondrial membrane. Taken together, these results indicate that PGAM5 suppresses mitochondrial energy expenditure by down-regulating UCP1 expression in brown adipocytes and that its phosphatase activity and intramembrane cleavage are required for UCP1 suppression.

Fabry disease is a heritable lipid disorder caused by the low activity of α-galactosidase A and characterized by the systemic accumulation of globotriaosylceramide (Gb3). Recent studies have reported a structural heterogeneity of Gb3 in Fabry disease, including Gb3 isoforms with different fatty acids and Gb3 analogs with modifications on the sphingosine moiety. However, Gb3 assays are often performed only on the selected Gb3 isoforms. To precisely determine the total Gb3 concentration, here we established two methods for determining both Gb3 isoforms and analogs. One was the deacylation method, involving Gb3 treatment with sphingolipid ceramide N-deacylase, followed by an assay of the deacylated products, globotriaosylsphingosine (lyso-Gb3) and its analogs, by ultra-performance LC coupled to tandem MS (UPLC-MS/MS). The other method was a direct assay established in the present study for 37 Gb3 isoforms and analogs/isoforms by UPLC-MS/MS. Gb3s from the organs of symptomatic animals of a Fabry disease mouse model were mainly Gb3 isoforms and two Gb3 analogs, such as Gb3(+18) containing the lyso-Gb3(+18) moiety and Gb3(−2) containing the lyso-Gb3(−2) moiety. The total concentrations and Gb3 analog distributions determined by the two methods were comparable. Gb3(+18) levels were high in the kidneys (24% of total Gb3) and the liver (13%), and we observed Gb3(−2) in the heart (10%) and the kidneys (5%). These results indicate organ-specific expression of Gb3 analogs, insights that may lead to a deeper understanding of the pathophysiology of Fabry disease.

The formation of translationally inactive 70S dimers (called 100S ribosomes) by hibernation-promoting factor is a widespread survival strategy among bacteria. Ribosome dimerization is thought to be reversible, with the dissociation of the 100S complexes enabling ribosome recycling for participation in new rounds of translation. The precise pathway of 100S ribosome recycling has been unclear. We previously found that the heat-shock GTPase HflX in the human pathogen Staphylococcus aureus is a minor disassembly factor. Cells lacking hflX do not accumulate 100S ribosomes unless they are subjected to heat exposure, suggesting the existence of an alternative pathway during nonstressed conditions. Here, we provide biochemical and genetic evidence that two essential translation factors, ribosome-recycling factor (RRF) and GTPase elongation factor G (EF-G), synergistically split 100S ribosomes in a GTP-dependent but tRNA translocation-independent manner. We found that although HflX and the RRF/EF-G pair are functionally interchangeable, HflX is expressed at low levels and is dispensable under normal growth conditions. The bacterial RRF/EF-G pair was previously known to target only the post-termination 70S complexes; our results reveal a new role in the reversal of ribosome hibernation that is intimately linked to bacterial pathogenesis, persister formation, stress responses, and ribosome integrity.

Coenzyme Q (Qn) is a vital lipid component of the electron transport chain that functions in cellular energy metabolism and as a membrane antioxidant. In the yeast Saccharomyces cerevisiae, coq1–coq9 deletion mutants are respiratory-incompetent, sensitive to lipid peroxidation stress, and unable to synthesize Q6. The yeast coq10 deletion mutant is also respiratory-deficient and sensitive to lipid peroxidation, yet it continues to produce Q6 at an impaired rate. Thus, Coq10 is required for the function of Q6 in respiration and as an antioxidant and is believed to chaperone Q6 from its site of synthesis to the respiratory complexes. In several fungi, Coq10 is encoded as a fusion polypeptide with Coq11, a recently identified protein of unknown function required for efficient Q6 biosynthesis. Because “fused” proteins are often involved in similar biochemical pathways, here we examined the putative functional relationship between Coq10 and Coq11 in yeast. We used plate growth and Seahorse assays and LC-MS/MS analysis to show that COQ11 deletion rescues respiratory deficiency, sensitivity to lipid peroxidation, and decreased Q6 biosynthesis of the coq10Δ mutant. Additionally, immunoblotting indicated that yeast coq11Δ mutants accumulate increased amounts of certain Coq polypeptides and display a stabilized CoQ synthome. These effects suggest that Coq11 modulates Q6 biosynthesis and that its absence increases mitochondrial Q6 content in the coq10Δcoq11Δ double mutant. This augmented mitochondrial Q6 content counteracts the respiratory deficiency and lipid peroxidation sensitivity phenotypes of the coq10Δ mutant. This study further clarifies the intricate connection between Q6 biosynthesis, trafficking, and function in mitochondrial metabolism.